TY  - CONF
AU  - Marinko, Marija
AU  - Janković, Goran
AU  - Milojević, Predrag
AU  - Stojanović, Ivan
AU  - Nenezić, Dragoslav
AU  - Kanjuh, Vladimir
AU  - Yang, Qin
AU  - He, Guo-Wei
AU  - Novaković, Aleksandra
PY  - 2022
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/4492
AB  - Findings from epidemiological studies indicate that polyphenols, widespread in
human diet and with numerous biological activities, act cardioprotectively. Procyanidins are
subclass of polyphenols with high content in commonly consumed foods and beverages, such
as grapes, tea, chocolate, nuts and apples. Cardioprotective abilities of procyanidins, might, at
least partly, attribute to their vasodilator properties. Since exact mechanisms of procyanidin
B2-induced vasorelaxation are unknown, our study aimed to investigate relaxant effect of
procyanidin B2 on isolated human saphenous vein (HSV) and its underlying mechanisms.
Discarded segments of HSV were collected from patients undergoing bypass surgery and
studied in organ baths. Procyanidin B2 caused concentration-dependent relaxation of HSV
precontracted by phenylephrine. The relaxation was strongly affected by inhibitors of
NO/cGMP pathway, L-NAME, hydroxocobalamin and ODQ. Indomethacin, a cyclooxygenase
inhibitor, significantly reduced only relaxation produced by the highest concentrations of
procyanidin B2. Combination of apamin and TRAM-34, selective blockers of small- and
intermediate-conductance Ca 2+ -activated K+ (KCa ) channels (SKCa and IK Ca ), in the presence of
L-NAME and indomethacin, did not additionally affect procyanidin B2-induced relaxation.
Additionally, relaxation induced by procyanidin B2 was partially attenuated by 4-
aminopyridine, predominant blocker of voltage-gated K+ (KV) channels, significantly
inhibited by glibenclamide, selective ATP-sensitive K+ (KATP) channels inhibitor, and almost
abolished by iberiotoxin, highly selective blocker of large-conductance KCa (BKCa ). Our results
revealed that procyanidin B2 acts as a potent vasodilator on isolated human venous graft.
Mechanism of this relaxation of HSV probably involves stimulation of NO production, as well
K+ channels opening, especially BK Ca , and partially KATP and KV
AB  - Nalazi epidemioloških studija ukazuju da polifenoli, široko rasprostranjeni u ljudskoj
ishrani i sa brojnim biološkim aktivnostima, deluju kardioprotektivno. Procijanidini su
podklasa polifenola sa visokim sadržajem u često konzumiranoj hrani i pićima, kao što su
grožđe, čaj, čokolada, orašasti plodovi i jabuke. Kardioprotektivno delovanje procijanidina
može se, bar delimično, pripisati njihovim vazodilatatornim svojstvima. S obzirom da tačni
mehanizmi pomoću kojih procijanidin B2 izaziva vazorelaksaciju nisu poznati, cilj naše
studije bio je da istražimo relaksantni efekat procijanidina B2 na izolovanoj humanoj veni
safeni (HSV) i njegove osnovne mehanizme.Neiskorišćeni segmenti HSV su uzimani od
pacijenata u toku bajpas operacija i ispitivani u kupatilu za izolovane organe. Procijanidin B2
izazvao je koncentracijski-zavisnu relaksaciju HSV prekontrahovane fenilefrinom. Na
relaksaciju su snažno uticali inhibitori NO/cGMP puta, L-NAME, hidroksokobalamin i ODQ.
Indometacin, inhibitor ciklooksigenaze, značajno je umanjio samo relaksaciju izazivanu
najvećim koncentracijama procijanidina B2. Kombinacija apamina i TRAM-34, selektivnih
blokatora Ca 2+ -zavisnih K+ (KCa ) kanala male i srednje provodljivosti (SKCa i IK Ca ), u prisustvu
L-NAME i indometacina, nije dodatno uticala na relaksaciju uzrokovanu procijanidinom B2.
Osim toga, procijanidinom B2 izazvana relaksacija bila je delimično umanjena 4-
aminopiridinom, dominantnim blokatorom voltažno-zavisnih K+ (KV) kanala, značajno
inhibirana glibenklamidom, selektivnim inhibitorom ATP-zavisnih K+ (KATP) kanala, i skoro
potpuno blokirana iberiotoksinom, selektivnim blokatorom K Ca velike provodljivosti (BK Ca).
Naši rezultati pokazuju da procijanidin B2 deluje kao moćni vazodilatator na izolovanom
humanom venskom graftu. Mehanizam ove relaksacije HSV verovatno uključuje stimulaciju
proizvodnje NO, kao i otvaranje K+ kanala, posebno BK Ca , i delimično KATP i KV
PB  - Savez farmaceutskih udruženja Srbije (SFUS)
C3  - Arhiv za farmaciju
T1  - Mechanism underlying vasorelaxation of human saphenous vein induced by procyanidin B2
T1  - Mehanizam vazorelaksacije humane vene safene izazvane procijanidinom B2
VL  - 72
IS  - 4 suplement
SP  - S190
EP  - S191
UR  - https://hdl.handle.net/21.15107/rcub_farfar_4492
ER  - 

@conference{
author = "Marinko, Marija and Janković, Goran and Milojević, Predrag and Stojanović, Ivan and Nenezić, Dragoslav and Kanjuh, Vladimir and Yang, Qin and He, Guo-Wei and Novaković, Aleksandra",
year = "2022",
abstract = "Findings from epidemiological studies indicate that polyphenols, widespread in
human diet and with numerous biological activities, act cardioprotectively. Procyanidins are
subclass of polyphenols with high content in commonly consumed foods and beverages, such
as grapes, tea, chocolate, nuts and apples. Cardioprotective abilities of procyanidins, might, at
least partly, attribute to their vasodilator properties. Since exact mechanisms of procyanidin
B2-induced vasorelaxation are unknown, our study aimed to investigate relaxant effect of
procyanidin B2 on isolated human saphenous vein (HSV) and its underlying mechanisms.
Discarded segments of HSV were collected from patients undergoing bypass surgery and
studied in organ baths. Procyanidin B2 caused concentration-dependent relaxation of HSV
precontracted by phenylephrine. The relaxation was strongly affected by inhibitors of
NO/cGMP pathway, L-NAME, hydroxocobalamin and ODQ. Indomethacin, a cyclooxygenase
inhibitor, significantly reduced only relaxation produced by the highest concentrations of
procyanidin B2. Combination of apamin and TRAM-34, selective blockers of small- and
intermediate-conductance Ca 2+ -activated K+ (KCa ) channels (SKCa and IK Ca ), in the presence of
L-NAME and indomethacin, did not additionally affect procyanidin B2-induced relaxation.
Additionally, relaxation induced by procyanidin B2 was partially attenuated by 4-
aminopyridine, predominant blocker of voltage-gated K+ (KV) channels, significantly
inhibited by glibenclamide, selective ATP-sensitive K+ (KATP) channels inhibitor, and almost
abolished by iberiotoxin, highly selective blocker of large-conductance KCa (BKCa ). Our results
revealed that procyanidin B2 acts as a potent vasodilator on isolated human venous graft.
Mechanism of this relaxation of HSV probably involves stimulation of NO production, as well
K+ channels opening, especially BK Ca , and partially KATP and KV, Nalazi epidemioloških studija ukazuju da polifenoli, široko rasprostranjeni u ljudskoj
ishrani i sa brojnim biološkim aktivnostima, deluju kardioprotektivno. Procijanidini su
podklasa polifenola sa visokim sadržajem u često konzumiranoj hrani i pićima, kao što su
grožđe, čaj, čokolada, orašasti plodovi i jabuke. Kardioprotektivno delovanje procijanidina
može se, bar delimično, pripisati njihovim vazodilatatornim svojstvima. S obzirom da tačni
mehanizmi pomoću kojih procijanidin B2 izaziva vazorelaksaciju nisu poznati, cilj naše
studije bio je da istražimo relaksantni efekat procijanidina B2 na izolovanoj humanoj veni
safeni (HSV) i njegove osnovne mehanizme.Neiskorišćeni segmenti HSV su uzimani od
pacijenata u toku bajpas operacija i ispitivani u kupatilu za izolovane organe. Procijanidin B2
izazvao je koncentracijski-zavisnu relaksaciju HSV prekontrahovane fenilefrinom. Na
relaksaciju su snažno uticali inhibitori NO/cGMP puta, L-NAME, hidroksokobalamin i ODQ.
Indometacin, inhibitor ciklooksigenaze, značajno je umanjio samo relaksaciju izazivanu
najvećim koncentracijama procijanidina B2. Kombinacija apamina i TRAM-34, selektivnih
blokatora Ca 2+ -zavisnih K+ (KCa ) kanala male i srednje provodljivosti (SKCa i IK Ca ), u prisustvu
L-NAME i indometacina, nije dodatno uticala na relaksaciju uzrokovanu procijanidinom B2.
Osim toga, procijanidinom B2 izazvana relaksacija bila je delimično umanjena 4-
aminopiridinom, dominantnim blokatorom voltažno-zavisnih K+ (KV) kanala, značajno
inhibirana glibenklamidom, selektivnim inhibitorom ATP-zavisnih K+ (KATP) kanala, i skoro
potpuno blokirana iberiotoksinom, selektivnim blokatorom K Ca velike provodljivosti (BK Ca).
Naši rezultati pokazuju da procijanidin B2 deluje kao moćni vazodilatator na izolovanom
humanom venskom graftu. Mehanizam ove relaksacije HSV verovatno uključuje stimulaciju
proizvodnje NO, kao i otvaranje K+ kanala, posebno BK Ca , i delimično KATP i KV",
publisher = "Savez farmaceutskih udruženja Srbije (SFUS)",
journal = "Arhiv za farmaciju",
title = "Mechanism underlying vasorelaxation of human saphenous vein induced by procyanidin B2, Mehanizam vazorelaksacije humane vene safene izazvane procijanidinom B2",
volume = "72",
number = "4 suplement",
pages = "S190-S191",
url = "https://hdl.handle.net/21.15107/rcub_farfar_4492"
}

Marinko, M., Janković, G., Milojević, P., Stojanović, I., Nenezić, D., Kanjuh, V., Yang, Q., He, G.,& Novaković, A.. (2022). Mechanism underlying vasorelaxation of human saphenous vein induced by procyanidin B2. in Arhiv za farmaciju
Savez farmaceutskih udruženja Srbije (SFUS)., 72(4 suplement), S190-S191.
https://hdl.handle.net/21.15107/rcub_farfar_4492

Marinko M, Janković G, Milojević P, Stojanović I, Nenezić D, Kanjuh V, Yang Q, He G, Novaković A. Mechanism underlying vasorelaxation of human saphenous vein induced by procyanidin B2. in Arhiv za farmaciju. 2022;72(4 suplement):S190-S191.
https://hdl.handle.net/21.15107/rcub_farfar_4492 .

Marinko, Marija, Janković, Goran, Milojević, Predrag, Stojanović, Ivan, Nenezić, Dragoslav, Kanjuh, Vladimir, Yang, Qin, He, Guo-Wei, Novaković, Aleksandra, "Mechanism underlying vasorelaxation of human saphenous vein induced by procyanidin B2" in Arhiv za farmaciju, 72, no. 4 suplement (2022):S190-S191,
https://hdl.handle.net/21.15107/rcub_farfar_4492 .

TY  - JOUR
AU  - Marinko, Marija
AU  - Hou, Hai-Tao
AU  - Stojanović, Ivan
AU  - Milojević, Predrag
AU  - Nenezić, Dragoslav
AU  - Kanjuh, Vladimir
AU  - Yang, Qin
AU  - He, Guo-Wei
AU  - Novaković, Aleksandra
PY  - 2021
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/3901
AB  - Hydrogen sulfide (H2S) represents the third and the youngest member of the gaseous transmitters family. The dominant effect of H2S on isolated vessels is vasodilation. As the mechanism of H2S-induced relaxation in human vessels remains unclear, the present study aimed to investigate the effects of H2S donor, sodium hydrosulfide (NaHS), on isolated human saphenous vein (HSV) and to determine the mechanism of action. Our results showed that NaHS (1 µM–3 mM) induced a concentration-dependent relaxation of endothelium-intact HSV rings pre-contracted by phenylephrine. Pre-treatment with L-NAME, ODQ and KT5823 significantly inhibited NaHS-induced relaxation, while indomethacin induced partial inhibition. Among K+ channel blockers, the combination of apamin and TRAM-34 significantly affected the relaxation produced by NaHS, while iberiotoxin and glibenclamide only reduced maximal relaxation of HSV. NaHS partially relaxed endothelium-intact rings pre-contracted by high K+, as well as phenylephrine-contracted rings in the presence of nifedipine. Additionally, the incubation of HSV rings with NaHS increased NO production. These results demonstrate that NaHS produces the concentration- and endothelium-dependent relaxation of isolated HSV. Vasorelaxation to NaHS probably involves activation of NO/cGMP/PKG pathway and partially prostacyclin. In addition, different K+ channels subtypes, especially SKCa and IKCa, as well as BKCa and KATP channels in high concentrations of NaHS, probably participate in the NaHS-induced vasorelaxation.
PB  - Blackwell Publishing Ltd
T2  - Fundamental and Clinical Pharmacology
T1  - Mechanisms underlying the vasorelaxant effect of hydrogen sulfide on human saphenous vein
VL  - 35
IS  - 5
SP  - 906
EP  - 918
DO  - 10.1111/fcp.12658
ER  - 

@article{
author = "Marinko, Marija and Hou, Hai-Tao and Stojanović, Ivan and Milojević, Predrag and Nenezić, Dragoslav and Kanjuh, Vladimir and Yang, Qin and He, Guo-Wei and Novaković, Aleksandra",
year = "2021",
abstract = "Hydrogen sulfide (H2S) represents the third and the youngest member of the gaseous transmitters family. The dominant effect of H2S on isolated vessels is vasodilation. As the mechanism of H2S-induced relaxation in human vessels remains unclear, the present study aimed to investigate the effects of H2S donor, sodium hydrosulfide (NaHS), on isolated human saphenous vein (HSV) and to determine the mechanism of action. Our results showed that NaHS (1 µM–3 mM) induced a concentration-dependent relaxation of endothelium-intact HSV rings pre-contracted by phenylephrine. Pre-treatment with L-NAME, ODQ and KT5823 significantly inhibited NaHS-induced relaxation, while indomethacin induced partial inhibition. Among K+ channel blockers, the combination of apamin and TRAM-34 significantly affected the relaxation produced by NaHS, while iberiotoxin and glibenclamide only reduced maximal relaxation of HSV. NaHS partially relaxed endothelium-intact rings pre-contracted by high K+, as well as phenylephrine-contracted rings in the presence of nifedipine. Additionally, the incubation of HSV rings with NaHS increased NO production. These results demonstrate that NaHS produces the concentration- and endothelium-dependent relaxation of isolated HSV. Vasorelaxation to NaHS probably involves activation of NO/cGMP/PKG pathway and partially prostacyclin. In addition, different K+ channels subtypes, especially SKCa and IKCa, as well as BKCa and KATP channels in high concentrations of NaHS, probably participate in the NaHS-induced vasorelaxation.",
publisher = "Blackwell Publishing Ltd",
journal = "Fundamental and Clinical Pharmacology",
title = "Mechanisms underlying the vasorelaxant effect of hydrogen sulfide on human saphenous vein",
volume = "35",
number = "5",
pages = "906-918",
doi = "10.1111/fcp.12658"
}

Marinko, M., Hou, H., Stojanović, I., Milojević, P., Nenezić, D., Kanjuh, V., Yang, Q., He, G.,& Novaković, A.. (2021). Mechanisms underlying the vasorelaxant effect of hydrogen sulfide on human saphenous vein. in Fundamental and Clinical Pharmacology
Blackwell Publishing Ltd., 35(5), 906-918.
https://doi.org/10.1111/fcp.12658

Marinko M, Hou H, Stojanović I, Milojević P, Nenezić D, Kanjuh V, Yang Q, He G, Novaković A. Mechanisms underlying the vasorelaxant effect of hydrogen sulfide on human saphenous vein. in Fundamental and Clinical Pharmacology. 2021;35(5):906-918.
doi:10.1111/fcp.12658 .

Marinko, Marija, Hou, Hai-Tao, Stojanović, Ivan, Milojević, Predrag, Nenezić, Dragoslav, Kanjuh, Vladimir, Yang, Qin, He, Guo-Wei, Novaković, Aleksandra, "Mechanisms underlying the vasorelaxant effect of hydrogen sulfide on human saphenous vein" in Fundamental and Clinical Pharmacology, 35, no. 5 (2021):906-918,
https://doi.org/10.1111/fcp.12658 . .

TY  - CONF
AU  - Novaković, Aleksandra
AU  - Marinko, Marija
AU  - Janković, Goran
AU  - Stojanović, Ivan
AU  - Milojević, Predrag
AU  - Nenezić, Dragoslav
AU  - Kanjuh, Vladimir
AU  - Yang, Qin
AU  - He, Guo-Wei
PY  - 2019
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/3260
PB  - Springer
C3  - European Journal of Clinical Pharmacology
T1  - Vasorelaxation of human saphenous vein induced by epicatechin
VL  - 75, Suppl. 1
SP  - S24
EP  - S24
DO  - 10.1007/s00228-019-02685-2
ER  - 

@conference{
author = "Novaković, Aleksandra and Marinko, Marija and Janković, Goran and Stojanović, Ivan and Milojević, Predrag and Nenezić, Dragoslav and Kanjuh, Vladimir and Yang, Qin and He, Guo-Wei",
year = "2019",
publisher = "Springer",
journal = "European Journal of Clinical Pharmacology",
title = "Vasorelaxation of human saphenous vein induced by epicatechin",
volume = "75, Suppl. 1",
pages = "S24-S24",
doi = "10.1007/s00228-019-02685-2"
}

Novaković, A., Marinko, M., Janković, G., Stojanović, I., Milojević, P., Nenezić, D., Kanjuh, V., Yang, Q.,& He, G.. (2019). Vasorelaxation of human saphenous vein induced by epicatechin. in European Journal of Clinical Pharmacology
Springer., 75, Suppl. 1, S24-S24.
https://doi.org/10.1007/s00228-019-02685-2

Novaković A, Marinko M, Janković G, Stojanović I, Milojević P, Nenezić D, Kanjuh V, Yang Q, He G. Vasorelaxation of human saphenous vein induced by epicatechin. in European Journal of Clinical Pharmacology. 2019;75, Suppl. 1:S24-S24.
doi:10.1007/s00228-019-02685-2 .

Novaković, Aleksandra, Marinko, Marija, Janković, Goran, Stojanović, Ivan, Milojević, Predrag, Nenezić, Dragoslav, Kanjuh, Vladimir, Yang, Qin, He, Guo-Wei, "Vasorelaxation of human saphenous vein induced by epicatechin" in European Journal of Clinical Pharmacology, 75, Suppl. 1 (2019):S24-S24,
https://doi.org/10.1007/s00228-019-02685-2 . .

TY  - JOUR
AU  - Janković, Goran
AU  - Marinko, Marija
AU  - Milojević, Predrag
AU  - Stojanović, Ivan
AU  - Nenezić, Dragoslav
AU  - Kanjuh, Vladimir
AU  - Yang, Qin
AU  - He, Guo-Wei
AU  - Novaković, Aleksandra
PY  - 2019
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/3515
AB  - Cardioprotective abilities of procyanidins, might, at least in part, attribute to their vasodilator properties. The present study was undertaken to assess the vasorelaxant effect of procyanidin B2 on isolated human saphenous vein (HSV) and its underlying mechanisms. Procyanidin B2 relaxed phenylephrine-induced contraction of HSV rings in concentration-dependent manner. The relaxation was dependent on the presence of endothelium and was strongly affected by l-NAME, hydroxocobalamin or ODQ, the inhibitors of NO/cGMP pathway. Indomethacin significantly affected only the relaxation produced by the highest concentrations of procyanidin B2. Apamin and TRAM-34 combination, in the presence of l-NAME and indomethacin, did not additionally decreased procyanidin B2-induced relaxation. In the presence of K+ channel blockers, relaxation induced by procyanidin B2 was partially attenuated by 4-aminopyridine, significantly inhibited by glibenclamide and almost abolished by iberiotoxin. Procyanidin B2 also relaxed the contractions induced by phenylephrine or caffeine in Ca2+-free solution. Finally, nifedipine slightly, while thapsigargin strongly antagonized HSV relaxation. Our results indicate that procyanidin B2 induces endothelium-dependent relaxation of HSV, which results primarily from stimulation of NO production, as well K+ channels opening, especially BKCa, and partially KATP and KV. Regulation of the intracellular Ca2+ release and inhibition of Ca2+ influx probably contr
PB  - Elsevier B.V.
T2  - Journal of Pharmacological Sciences
T1  - Mechanisms of endothelium-dependent vasorelaxation induced by procyanidin B2 in venous bypass graft
VL  - 142
IS  - 3
SP  - 101
EP  - 108
DO  - 10.1016/j.jphs.2019.11.006
ER  - 

@article{
author = "Janković, Goran and Marinko, Marija and Milojević, Predrag and Stojanović, Ivan and Nenezić, Dragoslav and Kanjuh, Vladimir and Yang, Qin and He, Guo-Wei and Novaković, Aleksandra",
year = "2019",
abstract = "Cardioprotective abilities of procyanidins, might, at least in part, attribute to their vasodilator properties. The present study was undertaken to assess the vasorelaxant effect of procyanidin B2 on isolated human saphenous vein (HSV) and its underlying mechanisms. Procyanidin B2 relaxed phenylephrine-induced contraction of HSV rings in concentration-dependent manner. The relaxation was dependent on the presence of endothelium and was strongly affected by l-NAME, hydroxocobalamin or ODQ, the inhibitors of NO/cGMP pathway. Indomethacin significantly affected only the relaxation produced by the highest concentrations of procyanidin B2. Apamin and TRAM-34 combination, in the presence of l-NAME and indomethacin, did not additionally decreased procyanidin B2-induced relaxation. In the presence of K+ channel blockers, relaxation induced by procyanidin B2 was partially attenuated by 4-aminopyridine, significantly inhibited by glibenclamide and almost abolished by iberiotoxin. Procyanidin B2 also relaxed the contractions induced by phenylephrine or caffeine in Ca2+-free solution. Finally, nifedipine slightly, while thapsigargin strongly antagonized HSV relaxation. Our results indicate that procyanidin B2 induces endothelium-dependent relaxation of HSV, which results primarily from stimulation of NO production, as well K+ channels opening, especially BKCa, and partially KATP and KV. Regulation of the intracellular Ca2+ release and inhibition of Ca2+ influx probably contr",
publisher = "Elsevier B.V.",
journal = "Journal of Pharmacological Sciences",
title = "Mechanisms of endothelium-dependent vasorelaxation induced by procyanidin B2 in venous bypass graft",
volume = "142",
number = "3",
pages = "101-108",
doi = "10.1016/j.jphs.2019.11.006"
}

Janković, G., Marinko, M., Milojević, P., Stojanović, I., Nenezić, D., Kanjuh, V., Yang, Q., He, G.,& Novaković, A.. (2019). Mechanisms of endothelium-dependent vasorelaxation induced by procyanidin B2 in venous bypass graft. in Journal of Pharmacological Sciences
Elsevier B.V.., 142(3), 101-108.
https://doi.org/10.1016/j.jphs.2019.11.006

Janković G, Marinko M, Milojević P, Stojanović I, Nenezić D, Kanjuh V, Yang Q, He G, Novaković A. Mechanisms of endothelium-dependent vasorelaxation induced by procyanidin B2 in venous bypass graft. in Journal of Pharmacological Sciences. 2019;142(3):101-108.
doi:10.1016/j.jphs.2019.11.006 .

Janković, Goran, Marinko, Marija, Milojević, Predrag, Stojanović, Ivan, Nenezić, Dragoslav, Kanjuh, Vladimir, Yang, Qin, He, Guo-Wei, Novaković, Aleksandra, "Mechanisms of endothelium-dependent vasorelaxation induced by procyanidin B2 in venous bypass graft" in Journal of Pharmacological Sciences, 142, no. 3 (2019):101-108,
https://doi.org/10.1016/j.jphs.2019.11.006 . .

TY  - JOUR
AU  - Sun, Wen-Tao
AU  - Wang, Xiang-Chong
AU  - Novaković, Aleksandra
AU  - Wang, Jun
AU  - He, Guo-Wei
AU  - Yang, Qin
PY  - 2019
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/3361
AB  - Objectives: We recently reported the involvement of ER stress-mediated BKCa channel inhibition in homocysteine-induced coronary dilator dysfunction. In another study, we demonstrated that tetramethylpyrazine (TMP), an active ingredient of the Chinese herb Chuanxiong, possesses potent anti-ER stress capacity. The present study investigated whether TMP protects BKCa channels from homocysteine-induced inhibition and whether suppression of ER stress is a mechanism contributing to the protection. Furthermore, we explored the signaling transduction involved in TMP-conferred protection on BKCa channels. Methods: BKCa channel-mediated relaxation was studied in porcine small coronary arteries. Expressions of BKCa channel subunits, ER stress molecules, and E3 ubiquitin ligases, as well as BKCa ubiquitination were determined in porcine coronary arterial smooth muscle cells (PCASMCs). Whole-cell BKCa currents were recorded. Results: Exposure of PCASMCs to homocysteine or the chemical ER stressor tunicamycin increased the expression of ER stress molecules, which was significantly inhibited by TMP. Suppression of ER stress by TMP preserved the BKCa beta 1 protein level and restored the BKCa current in PCASMCs, concomitant with an improved BKCa mediated dilatation in coronary arteries. TMP attenuated homocysteine-induced BKCa beta 1 protein ubiquitination, in which inhibition of ER stress-mediated FoxO3a activation and FoxO3a-dependent atrogin-1 and Murf-1 was involved. Conclusions: Reversal of BKCa channel inhibition via suppressing ER stress-mediated loss of beta 1 subunits contributes to the protective effect of TMP against homocysteine on coronary dilator function. Inhibition of FoxO3a-dependent ubiquitin ligases is involved in TMP-conferred normalization of BKCa beta 1 protein level. These results provide new mechanistic insights into the cardiovascular benefits of TMP.
PB  - Elsevier Science Inc, New York
T2  - Vibrational Spectroscopy
T1  - Protection of dilator function of coronary arteries from homocysteine by tetramethylpyrazine: Role of ER stress in modulation of BKCa channels
VL  - 113
SP  - 27
EP  - 37
DO  - 10.1016/j.vph.2018.10.009
ER  - 

@article{
author = "Sun, Wen-Tao and Wang, Xiang-Chong and Novaković, Aleksandra and Wang, Jun and He, Guo-Wei and Yang, Qin",
year = "2019",
abstract = "Objectives: We recently reported the involvement of ER stress-mediated BKCa channel inhibition in homocysteine-induced coronary dilator dysfunction. In another study, we demonstrated that tetramethylpyrazine (TMP), an active ingredient of the Chinese herb Chuanxiong, possesses potent anti-ER stress capacity. The present study investigated whether TMP protects BKCa channels from homocysteine-induced inhibition and whether suppression of ER stress is a mechanism contributing to the protection. Furthermore, we explored the signaling transduction involved in TMP-conferred protection on BKCa channels. Methods: BKCa channel-mediated relaxation was studied in porcine small coronary arteries. Expressions of BKCa channel subunits, ER stress molecules, and E3 ubiquitin ligases, as well as BKCa ubiquitination were determined in porcine coronary arterial smooth muscle cells (PCASMCs). Whole-cell BKCa currents were recorded. Results: Exposure of PCASMCs to homocysteine or the chemical ER stressor tunicamycin increased the expression of ER stress molecules, which was significantly inhibited by TMP. Suppression of ER stress by TMP preserved the BKCa beta 1 protein level and restored the BKCa current in PCASMCs, concomitant with an improved BKCa mediated dilatation in coronary arteries. TMP attenuated homocysteine-induced BKCa beta 1 protein ubiquitination, in which inhibition of ER stress-mediated FoxO3a activation and FoxO3a-dependent atrogin-1 and Murf-1 was involved. Conclusions: Reversal of BKCa channel inhibition via suppressing ER stress-mediated loss of beta 1 subunits contributes to the protective effect of TMP against homocysteine on coronary dilator function. Inhibition of FoxO3a-dependent ubiquitin ligases is involved in TMP-conferred normalization of BKCa beta 1 protein level. These results provide new mechanistic insights into the cardiovascular benefits of TMP.",
publisher = "Elsevier Science Inc, New York",
journal = "Vibrational Spectroscopy",
title = "Protection of dilator function of coronary arteries from homocysteine by tetramethylpyrazine: Role of ER stress in modulation of BKCa channels",
volume = "113",
pages = "27-37",
doi = "10.1016/j.vph.2018.10.009"
}

Sun, W., Wang, X., Novaković, A., Wang, J., He, G.,& Yang, Q.. (2019). Protection of dilator function of coronary arteries from homocysteine by tetramethylpyrazine: Role of ER stress in modulation of BKCa channels. in Vibrational Spectroscopy
Elsevier Science Inc, New York., 113, 27-37.
https://doi.org/10.1016/j.vph.2018.10.009

Sun W, Wang X, Novaković A, Wang J, He G, Yang Q. Protection of dilator function of coronary arteries from homocysteine by tetramethylpyrazine: Role of ER stress in modulation of BKCa channels. in Vibrational Spectroscopy. 2019;113:27-37.
doi:10.1016/j.vph.2018.10.009 .

Sun, Wen-Tao, Wang, Xiang-Chong, Novaković, Aleksandra, Wang, Jun, He, Guo-Wei, Yang, Qin, "Protection of dilator function of coronary arteries from homocysteine by tetramethylpyrazine: Role of ER stress in modulation of BKCa channels" in Vibrational Spectroscopy, 113 (2019):27-37,
https://doi.org/10.1016/j.vph.2018.10.009 . .

TY  - CONF
AU  - Novaković, Aleksandra
AU  - Marinko, Marija
AU  - Janković, Goran
AU  - Nenezić, Dragoslav
AU  - Stojanović, Ivan
AU  - Milojević, Predrag
AU  - Kanjuh, Vladimir
AU  - Yang, Qin
AU  - He, Guo-Wei
PY  - 2018
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/3072
PB  - Elsevier Ireland Ltd, Clare
C3  - Atherosclerosis
T1  - Cardioprotective effect of procyanidin B2
VL  - 275
SP  - e72
EP  - e72
DO  - 10.1016/j.atherosclerosis.2018.06.200
ER  - 

@conference{
author = "Novaković, Aleksandra and Marinko, Marija and Janković, Goran and Nenezić, Dragoslav and Stojanović, Ivan and Milojević, Predrag and Kanjuh, Vladimir and Yang, Qin and He, Guo-Wei",
year = "2018",
publisher = "Elsevier Ireland Ltd, Clare",
journal = "Atherosclerosis",
title = "Cardioprotective effect of procyanidin B2",
volume = "275",
pages = "e72-e72",
doi = "10.1016/j.atherosclerosis.2018.06.200"
}

Novaković, A., Marinko, M., Janković, G., Nenezić, D., Stojanović, I., Milojević, P., Kanjuh, V., Yang, Q.,& He, G.. (2018). Cardioprotective effect of procyanidin B2. in Atherosclerosis
Elsevier Ireland Ltd, Clare., 275, e72-e72.
https://doi.org/10.1016/j.atherosclerosis.2018.06.200

Novaković A, Marinko M, Janković G, Nenezić D, Stojanović I, Milojević P, Kanjuh V, Yang Q, He G. Cardioprotective effect of procyanidin B2. in Atherosclerosis. 2018;275:e72-e72.
doi:10.1016/j.atherosclerosis.2018.06.200 .

Novaković, Aleksandra, Marinko, Marija, Janković, Goran, Nenezić, Dragoslav, Stojanović, Ivan, Milojević, Predrag, Kanjuh, Vladimir, Yang, Qin, He, Guo-Wei, "Cardioprotective effect of procyanidin B2" in Atherosclerosis, 275 (2018):e72-e72,
https://doi.org/10.1016/j.atherosclerosis.2018.06.200 . .

TY  - JOUR
AU  - Novaković, Aleksandra
AU  - Marinko, Marija
AU  - Janković, Goran
AU  - Stojanović, Ivan
AU  - Milojević, Predrag
AU  - Nenezić, Dragoslav
AU  - Kanjuh, Vladimir
AU  - Yang, Qin
AU  - He, Guo-Wei
PY  - 2017
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/2972
AB  - The aim of the present study was to investigate and characterize vasorelaxant effect of procyanidin B2 on human internal mammary artery (HIMA) as one of the mechanisms of its protective effect against vascular risk. Procyanidin B2 induced strong concentration-dependent relaxation of HIMA rings pre-contracted by phenylephrine. Pretreatment with L-NAME, a NO synthase inhibitor, hydroxocobalamin, a NO scavenger, and ODQ, an inhibitor of soluble guanylate cyclase, significantly inhibited procyanidin B2-induced relaxation of HIMA, while indomethacin, a cyclooxygenase inhibitor, considerably reduced effects of low concentrations. Among K+ channel blockers, iberiotoxin, a selective blocker of large conductance Ca2+-activated K+ channels (BKCa), abolished procyanidin B2-induced relaxation, glibenclamide, a selective ATP-sensitive K+(K-ATP) channels blocker, induced partial inhibition, while 4-aminopyridine, a blocker of voltage-gated K+(K-V) channels, and TRAM-34, an inhibitor of intermediate-conductance Ca2+-activated K+(IKCa) channels, slightly reduced maximal relaxation of HIMA. Further, procyanidin B2 relaxed contraction induced by phenylephrine in Ca2+-free Krebs solution, but had no effect on contraction induced by caffeine. Finally, thapsigargin, a sarcoplasmic reticulum Ca2+-ATPase inhibitor, significantly reduced relaxation of HIMA produced by procyanidin B2. These results demonstrate that procyanidin B2 produces endothelium-dependent relaxation of HIMA pre-contracted by phenylephrine. This effect is primarily the result of an increased NO synthesis and secretion by endothelial cells and partially of prostacyclin, although it involves activation of BKCa and K-ATP, as well as K-V and IKCa channels in high concentrations of procyanidin B2.
PB  - Elsevier Science BV, Amsterdam
T2  - European Journal of Pharmacology
T1  - Endothelium-dependent vasorelaxant effect of procyanidin B2 on human internal mammary artery
VL  - 807
SP  - 75
EP  - 81
DO  - 10.1016/j.ejphar.2017.04.015
ER  - 

@article{
author = "Novaković, Aleksandra and Marinko, Marija and Janković, Goran and Stojanović, Ivan and Milojević, Predrag and Nenezić, Dragoslav and Kanjuh, Vladimir and Yang, Qin and He, Guo-Wei",
year = "2017",
abstract = "The aim of the present study was to investigate and characterize vasorelaxant effect of procyanidin B2 on human internal mammary artery (HIMA) as one of the mechanisms of its protective effect against vascular risk. Procyanidin B2 induced strong concentration-dependent relaxation of HIMA rings pre-contracted by phenylephrine. Pretreatment with L-NAME, a NO synthase inhibitor, hydroxocobalamin, a NO scavenger, and ODQ, an inhibitor of soluble guanylate cyclase, significantly inhibited procyanidin B2-induced relaxation of HIMA, while indomethacin, a cyclooxygenase inhibitor, considerably reduced effects of low concentrations. Among K+ channel blockers, iberiotoxin, a selective blocker of large conductance Ca2+-activated K+ channels (BKCa), abolished procyanidin B2-induced relaxation, glibenclamide, a selective ATP-sensitive K+(K-ATP) channels blocker, induced partial inhibition, while 4-aminopyridine, a blocker of voltage-gated K+(K-V) channels, and TRAM-34, an inhibitor of intermediate-conductance Ca2+-activated K+(IKCa) channels, slightly reduced maximal relaxation of HIMA. Further, procyanidin B2 relaxed contraction induced by phenylephrine in Ca2+-free Krebs solution, but had no effect on contraction induced by caffeine. Finally, thapsigargin, a sarcoplasmic reticulum Ca2+-ATPase inhibitor, significantly reduced relaxation of HIMA produced by procyanidin B2. These results demonstrate that procyanidin B2 produces endothelium-dependent relaxation of HIMA pre-contracted by phenylephrine. This effect is primarily the result of an increased NO synthesis and secretion by endothelial cells and partially of prostacyclin, although it involves activation of BKCa and K-ATP, as well as K-V and IKCa channels in high concentrations of procyanidin B2.",
publisher = "Elsevier Science BV, Amsterdam",
journal = "European Journal of Pharmacology",
title = "Endothelium-dependent vasorelaxant effect of procyanidin B2 on human internal mammary artery",
volume = "807",
pages = "75-81",
doi = "10.1016/j.ejphar.2017.04.015"
}

Novaković, A., Marinko, M., Janković, G., Stojanović, I., Milojević, P., Nenezić, D., Kanjuh, V., Yang, Q.,& He, G.. (2017). Endothelium-dependent vasorelaxant effect of procyanidin B2 on human internal mammary artery. in European Journal of Pharmacology
Elsevier Science BV, Amsterdam., 807, 75-81.
https://doi.org/10.1016/j.ejphar.2017.04.015

Novaković A, Marinko M, Janković G, Stojanović I, Milojević P, Nenezić D, Kanjuh V, Yang Q, He G. Endothelium-dependent vasorelaxant effect of procyanidin B2 on human internal mammary artery. in European Journal of Pharmacology. 2017;807:75-81.
doi:10.1016/j.ejphar.2017.04.015 .

Novaković, Aleksandra, Marinko, Marija, Janković, Goran, Stojanović, Ivan, Milojević, Predrag, Nenezić, Dragoslav, Kanjuh, Vladimir, Yang, Qin, He, Guo-Wei, "Endothelium-dependent vasorelaxant effect of procyanidin B2 on human internal mammary artery" in European Journal of Pharmacology, 807 (2017):75-81,
https://doi.org/10.1016/j.ejphar.2017.04.015 . .

TY  - JOUR
AU  - Hou, Hai-Tao
AU  - Wang, Jun
AU  - Wang, Zheng-Qing
AU  - Liu, Xiao-Cheng
AU  - Marinko, Marija
AU  - Novaković, Aleksandra
AU  - Yang, Qin
AU  - He, Guo-Wei
PY  - 2016
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/2525
AB  - Background. Graft spasm remains challenging in coronary artery bypass grafting (CABG). Calcium antagonists are commonly used in patients with coronary artery disease. This study investigated the inhibitory effect of third-generation dihydropyridine calcium channel antagonist benidipine on the vasoconstriction induced by various vasoconstrictors in the human internalmammary artery(IMA). Methods. Isolated human IMA rings (N = 65, taken from 37 patients undergoing CABG) were studied in a myograph in 2 ways: the relaxing effect of benidipine on vasoconstrictor-induced precontraction by KCl and U46619 and the depressing effect of benidipine at plasma concentrations on the contraction. Enzyme-linked immunosorbent assay (ELISA) was used to measure the change of the protein related to the L-type calcium channel. Results. Benidipine caused more relaxation in KCl-contracted (86.7% +/- 3.3%; n = 12) than in U46619-contracted (63.8% +/- 5.3%; n = 8; p  lt  0.001) IMA rings. Pretreatment of IMA with plasma concentrations of benidipine (-6.92 log M) significantly depressed subsequent contraction by KCl (from 17.3 +/- 2.7 mN to 7.4 +/- 1.2 mN; n = 6; p  lt  0.05) but did not significantly affect the contraction caused by U46619. Benidipine also caused a decrease of caveolin (CaV) 1.2 protein content (0.55 +/- 0.02 versus 0.63 +/- 0.02 mg/mL; p  lt  0.05). Conclusions. We conclude that in human IMA, the third-generation dihydropyridine calcium channel antagonist benidipine has a potent inhibitory effect on the vasoconstriction mediated by a variety of vasoconstrictors. Use of benidipine in patients undergoing CABG may provide vasorelaxant or antispastic effects in the grafts.
PB  - Elsevier Science Inc, New York
T2  - Annals of Thoracic Surgery
T1  - Effect of Benidipine in Human Internal Mammary Artery and Clinical Implications
VL  - 101
IS  - 5
SP  - 1789
EP  - 1795
DO  - 10.1016/j.athoracsur.2015.10.029
ER  - 

@article{
author = "Hou, Hai-Tao and Wang, Jun and Wang, Zheng-Qing and Liu, Xiao-Cheng and Marinko, Marija and Novaković, Aleksandra and Yang, Qin and He, Guo-Wei",
year = "2016",
abstract = "Background. Graft spasm remains challenging in coronary artery bypass grafting (CABG). Calcium antagonists are commonly used in patients with coronary artery disease. This study investigated the inhibitory effect of third-generation dihydropyridine calcium channel antagonist benidipine on the vasoconstriction induced by various vasoconstrictors in the human internalmammary artery(IMA). Methods. Isolated human IMA rings (N = 65, taken from 37 patients undergoing CABG) were studied in a myograph in 2 ways: the relaxing effect of benidipine on vasoconstrictor-induced precontraction by KCl and U46619 and the depressing effect of benidipine at plasma concentrations on the contraction. Enzyme-linked immunosorbent assay (ELISA) was used to measure the change of the protein related to the L-type calcium channel. Results. Benidipine caused more relaxation in KCl-contracted (86.7% +/- 3.3%; n = 12) than in U46619-contracted (63.8% +/- 5.3%; n = 8; p  lt  0.001) IMA rings. Pretreatment of IMA with plasma concentrations of benidipine (-6.92 log M) significantly depressed subsequent contraction by KCl (from 17.3 +/- 2.7 mN to 7.4 +/- 1.2 mN; n = 6; p  lt  0.05) but did not significantly affect the contraction caused by U46619. Benidipine also caused a decrease of caveolin (CaV) 1.2 protein content (0.55 +/- 0.02 versus 0.63 +/- 0.02 mg/mL; p  lt  0.05). Conclusions. We conclude that in human IMA, the third-generation dihydropyridine calcium channel antagonist benidipine has a potent inhibitory effect on the vasoconstriction mediated by a variety of vasoconstrictors. Use of benidipine in patients undergoing CABG may provide vasorelaxant or antispastic effects in the grafts.",
publisher = "Elsevier Science Inc, New York",
journal = "Annals of Thoracic Surgery",
title = "Effect of Benidipine in Human Internal Mammary Artery and Clinical Implications",
volume = "101",
number = "5",
pages = "1789-1795",
doi = "10.1016/j.athoracsur.2015.10.029"
}

Hou, H., Wang, J., Wang, Z., Liu, X., Marinko, M., Novaković, A., Yang, Q.,& He, G.. (2016). Effect of Benidipine in Human Internal Mammary Artery and Clinical Implications. in Annals of Thoracic Surgery
Elsevier Science Inc, New York., 101(5), 1789-1795.
https://doi.org/10.1016/j.athoracsur.2015.10.029

Hou H, Wang J, Wang Z, Liu X, Marinko M, Novaković A, Yang Q, He G. Effect of Benidipine in Human Internal Mammary Artery and Clinical Implications. in Annals of Thoracic Surgery. 2016;101(5):1789-1795.
doi:10.1016/j.athoracsur.2015.10.029 .

Hou, Hai-Tao, Wang, Jun, Wang, Zheng-Qing, Liu, Xiao-Cheng, Marinko, Marija, Novaković, Aleksandra, Yang, Qin, He, Guo-Wei, "Effect of Benidipine in Human Internal Mammary Artery and Clinical Implications" in Annals of Thoracic Surgery, 101, no. 5 (2016):1789-1795,
https://doi.org/10.1016/j.athoracsur.2015.10.029 . .

TY  - CONF
AU  - Novaković, Aleksandra
AU  - Marinko, Marija
AU  - Vranić, Aleksandra
AU  - Janković, Goran
AU  - Stojanović, Ivan
AU  - Milojević, Predrag
AU  - Ugrešić, Nenad
AU  - Kanjuh, Vladimir
AU  - Yang, Qin
AU  - He, Guo-Wei
PY  - 2015
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/2442
PB  - Elsevier Ireland Ltd, Clare
C3  - Atherosclerosis
T1  - Epicatechin induced vasorelaxation of human internal mammary artery
VL  - 241
IS  - 1
SP  - e50
EP  - e50
DO  - 10.1016/j.atherosclerosis.2015.04.178
ER  - 

@conference{
author = "Novaković, Aleksandra and Marinko, Marija and Vranić, Aleksandra and Janković, Goran and Stojanović, Ivan and Milojević, Predrag and Ugrešić, Nenad and Kanjuh, Vladimir and Yang, Qin and He, Guo-Wei",
year = "2015",
publisher = "Elsevier Ireland Ltd, Clare",
journal = "Atherosclerosis",
title = "Epicatechin induced vasorelaxation of human internal mammary artery",
volume = "241",
number = "1",
pages = "e50-e50",
doi = "10.1016/j.atherosclerosis.2015.04.178"
}

Novaković, A., Marinko, M., Vranić, A., Janković, G., Stojanović, I., Milojević, P., Ugrešić, N., Kanjuh, V., Yang, Q.,& He, G.. (2015). Epicatechin induced vasorelaxation of human internal mammary artery. in Atherosclerosis
Elsevier Ireland Ltd, Clare., 241(1), e50-e50.
https://doi.org/10.1016/j.atherosclerosis.2015.04.178

Novaković A, Marinko M, Vranić A, Janković G, Stojanović I, Milojević P, Ugrešić N, Kanjuh V, Yang Q, He G. Epicatechin induced vasorelaxation of human internal mammary artery. in Atherosclerosis. 2015;241(1):e50-e50.
doi:10.1016/j.atherosclerosis.2015.04.178 .

Novaković, Aleksandra, Marinko, Marija, Vranić, Aleksandra, Janković, Goran, Stojanović, Ivan, Milojević, Predrag, Ugrešić, Nenad, Kanjuh, Vladimir, Yang, Qin, He, Guo-Wei, "Epicatechin induced vasorelaxation of human internal mammary artery" in Atherosclerosis, 241, no. 1 (2015):e50-e50,
https://doi.org/10.1016/j.atherosclerosis.2015.04.178 . .

TY  - JOUR
AU  - Marinko, Marija
AU  - Novaković, Aleksandra
AU  - Nenezić, Dragoslav
AU  - Stojanović, Ivan
AU  - Milojević, Predrag
AU  - Jović, Miomir
AU  - Ugrešić, Nenad
AU  - Kanjuh, Vladimir
AU  - Yang, Qin
AU  - He, Guo-Wei
PY  - 2015
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/2461
AB  - As we previously demonstrated the role of different K+ channels in the action of nicorandil on human saphenous vein (HSV) and human internal mammary artery (HIMA), this study aimed to analyse the contribution of the cGMP pathway in nicorandil-induced vasorelaxation and to determine the involvement of cGMP in the K+ channel-activating effect of nicorandil. An inhibitor of soluble guanylate cyclase (GC), ODQ, significantly inhibited nicorandil-induced relaxation, while ODQ plus glibenclamide, a selective ATP-sensitive K+ (KATP) channel inhibitor, produced a further inhibition of both vessels. In HSV, ODQ in combination with 4-aminopyridine, a blocker of voltage-gated K+ (K-V) channels, did not modify the concentration-response to nicorandil compared with ODQ, whereas in HIMA, ODQ plus iberiotoxin, a selective blocker of large-conductance Ca2+-activated K+ (BKCa) channels, produced greater inhibition than ODQ alone. We showed that the cGMP pathway plays a significant role in the vasorelaxant effect of nicorandil on HSV and HIMA. It seems that nicorandil directly opens KATP channels in both vessels and BKCa channels in HIMA, although it is possible that stimulation of GC contributes to KATP channels activation in HIMA. Contrary, the activation of K-V channels in HSV is probably due to GC activation and increased levels of cGMP.
PB  - Japanese Pharmacological Soc, Kyoto
T2  - Journal of Pharmacological Sciences
T1  - Nicorandil directly and cyclic GMP-dependently opens K+ channels in human bypass grafts
VL  - 128
IS  - 2
SP  - 59
EP  - 64
DO  - 10.1016/j.jphs.2015.03.003
ER  - 

@article{
author = "Marinko, Marija and Novaković, Aleksandra and Nenezić, Dragoslav and Stojanović, Ivan and Milojević, Predrag and Jović, Miomir and Ugrešić, Nenad and Kanjuh, Vladimir and Yang, Qin and He, Guo-Wei",
year = "2015",
abstract = "As we previously demonstrated the role of different K+ channels in the action of nicorandil on human saphenous vein (HSV) and human internal mammary artery (HIMA), this study aimed to analyse the contribution of the cGMP pathway in nicorandil-induced vasorelaxation and to determine the involvement of cGMP in the K+ channel-activating effect of nicorandil. An inhibitor of soluble guanylate cyclase (GC), ODQ, significantly inhibited nicorandil-induced relaxation, while ODQ plus glibenclamide, a selective ATP-sensitive K+ (KATP) channel inhibitor, produced a further inhibition of both vessels. In HSV, ODQ in combination with 4-aminopyridine, a blocker of voltage-gated K+ (K-V) channels, did not modify the concentration-response to nicorandil compared with ODQ, whereas in HIMA, ODQ plus iberiotoxin, a selective blocker of large-conductance Ca2+-activated K+ (BKCa) channels, produced greater inhibition than ODQ alone. We showed that the cGMP pathway plays a significant role in the vasorelaxant effect of nicorandil on HSV and HIMA. It seems that nicorandil directly opens KATP channels in both vessels and BKCa channels in HIMA, although it is possible that stimulation of GC contributes to KATP channels activation in HIMA. Contrary, the activation of K-V channels in HSV is probably due to GC activation and increased levels of cGMP.",
publisher = "Japanese Pharmacological Soc, Kyoto",
journal = "Journal of Pharmacological Sciences",
title = "Nicorandil directly and cyclic GMP-dependently opens K+ channels in human bypass grafts",
volume = "128",
number = "2",
pages = "59-64",
doi = "10.1016/j.jphs.2015.03.003"
}

Marinko, M., Novaković, A., Nenezić, D., Stojanović, I., Milojević, P., Jović, M., Ugrešić, N., Kanjuh, V., Yang, Q.,& He, G.. (2015). Nicorandil directly and cyclic GMP-dependently opens K+ channels in human bypass grafts. in Journal of Pharmacological Sciences
Japanese Pharmacological Soc, Kyoto., 128(2), 59-64.
https://doi.org/10.1016/j.jphs.2015.03.003

Marinko M, Novaković A, Nenezić D, Stojanović I, Milojević P, Jović M, Ugrešić N, Kanjuh V, Yang Q, He G. Nicorandil directly and cyclic GMP-dependently opens K+ channels in human bypass grafts. in Journal of Pharmacological Sciences. 2015;128(2):59-64.
doi:10.1016/j.jphs.2015.03.003 .

Marinko, Marija, Novaković, Aleksandra, Nenezić, Dragoslav, Stojanović, Ivan, Milojević, Predrag, Jović, Miomir, Ugrešić, Nenad, Kanjuh, Vladimir, Yang, Qin, He, Guo-Wei, "Nicorandil directly and cyclic GMP-dependently opens K+ channels in human bypass grafts" in Journal of Pharmacological Sciences, 128, no. 2 (2015):59-64,
https://doi.org/10.1016/j.jphs.2015.03.003 . .

TY  - JOUR
AU  - Novaković, Aleksandra
AU  - Marinko, Marija
AU  - Vranić, Aleksandra
AU  - Janković, Goran
AU  - Milojević, Predrag
AU  - Stojanović, Ivan
AU  - Nenezić, Dragoslav
AU  - Ugrešić, Nenad
AU  - Kanjuh, Vladimir
AU  - Yang, Qin
AU  - He, Guo-Wei
PY  - 2015
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/2439
AB  - Evidences have suggested that flavanol compound (-)-epicatechin is associated with reduced risk of cardiovascular diseases. One of the mechanisms of its cardioprotective effect is vasodilation. However, the exact mechanisms by which (-)-epicatechin causes vasodilation are not yet clearly defined. The aims of the present study were to investigate relaxant effect of flavanol (-)-epicatechin on the isolated human internal mammary artery (HIMA) and to determine the mechanisms underlying its vasorelaxation. Our results showed that (-)-epicatechin induced a concentration-dependent relaxation of RNA rings pre-contracted by phenylephrine. Among the K+ channel blockers, 4-aminopyricline (4-AP) and margatoxin, blockers of voltage gated K+ (K-V) channels, and glibenclamide, a selective ATP sensitive K+ (K-ATP,) channels blocker, partly inhibited the (-)-epicatechin-induced relaxation of HIMA, while iberiotoxin, a most selective blocker of large conductance Ca2+-activated K+ channels (BKCa), almost completely inhibited the relaxation. In rings pre-contracted by 80 mM K+, (-)-epicatechin induced partial relaxation of HIMA, whereas in Ca2+-free medium, (-)-epicatechin completely relaxed HIMA rings pre-contracted by phenylephrine and caffeine. Finally, thapsigargin, a sarcoplasmic reticulum Ca2+-ATPase inhibitor, slightly antagonized (-)-epicatechin-induced relaxation of HIMA pre-contracted by phenylephrine. These results suggest that (-)-epicatechin induces strong endothelium independent relaxation of HIMA pre-contracted by phenylephrine whilst 4-AP- and rnargatoxin-sensitive K-V channels, as well as BKCa and K-ATP channels, located in vascular smooth muscle, mediate this relaxation. In addition, it seems that (-)-epicatechin could inhibit influx of extracellular Ca2+, interfere with intracellular Ca2+ release and re uptake by the sarcoplasmic reticulum.
PB  - Elsevier Science BV, Amsterdam
T2  - European Journal of Pharmacology
T1  - Mechanisms underlying the vasorelaxation of human internal mammary artery induced by (-)-epicatechin
VL  - 762
SP  - 306
EP  - 312
DO  - 10.1016/j.ejphar.2015.05.066
ER  - 

@article{
author = "Novaković, Aleksandra and Marinko, Marija and Vranić, Aleksandra and Janković, Goran and Milojević, Predrag and Stojanović, Ivan and Nenezić, Dragoslav and Ugrešić, Nenad and Kanjuh, Vladimir and Yang, Qin and He, Guo-Wei",
year = "2015",
abstract = "Evidences have suggested that flavanol compound (-)-epicatechin is associated with reduced risk of cardiovascular diseases. One of the mechanisms of its cardioprotective effect is vasodilation. However, the exact mechanisms by which (-)-epicatechin causes vasodilation are not yet clearly defined. The aims of the present study were to investigate relaxant effect of flavanol (-)-epicatechin on the isolated human internal mammary artery (HIMA) and to determine the mechanisms underlying its vasorelaxation. Our results showed that (-)-epicatechin induced a concentration-dependent relaxation of RNA rings pre-contracted by phenylephrine. Among the K+ channel blockers, 4-aminopyricline (4-AP) and margatoxin, blockers of voltage gated K+ (K-V) channels, and glibenclamide, a selective ATP sensitive K+ (K-ATP,) channels blocker, partly inhibited the (-)-epicatechin-induced relaxation of HIMA, while iberiotoxin, a most selective blocker of large conductance Ca2+-activated K+ channels (BKCa), almost completely inhibited the relaxation. In rings pre-contracted by 80 mM K+, (-)-epicatechin induced partial relaxation of HIMA, whereas in Ca2+-free medium, (-)-epicatechin completely relaxed HIMA rings pre-contracted by phenylephrine and caffeine. Finally, thapsigargin, a sarcoplasmic reticulum Ca2+-ATPase inhibitor, slightly antagonized (-)-epicatechin-induced relaxation of HIMA pre-contracted by phenylephrine. These results suggest that (-)-epicatechin induces strong endothelium independent relaxation of HIMA pre-contracted by phenylephrine whilst 4-AP- and rnargatoxin-sensitive K-V channels, as well as BKCa and K-ATP channels, located in vascular smooth muscle, mediate this relaxation. In addition, it seems that (-)-epicatechin could inhibit influx of extracellular Ca2+, interfere with intracellular Ca2+ release and re uptake by the sarcoplasmic reticulum.",
publisher = "Elsevier Science BV, Amsterdam",
journal = "European Journal of Pharmacology",
title = "Mechanisms underlying the vasorelaxation of human internal mammary artery induced by (-)-epicatechin",
volume = "762",
pages = "306-312",
doi = "10.1016/j.ejphar.2015.05.066"
}

Novaković, A., Marinko, M., Vranić, A., Janković, G., Milojević, P., Stojanović, I., Nenezić, D., Ugrešić, N., Kanjuh, V., Yang, Q.,& He, G.. (2015). Mechanisms underlying the vasorelaxation of human internal mammary artery induced by (-)-epicatechin. in European Journal of Pharmacology
Elsevier Science BV, Amsterdam., 762, 306-312.
https://doi.org/10.1016/j.ejphar.2015.05.066

Novaković A, Marinko M, Vranić A, Janković G, Milojević P, Stojanović I, Nenezić D, Ugrešić N, Kanjuh V, Yang Q, He G. Mechanisms underlying the vasorelaxation of human internal mammary artery induced by (-)-epicatechin. in European Journal of Pharmacology. 2015;762:306-312.
doi:10.1016/j.ejphar.2015.05.066 .

Novaković, Aleksandra, Marinko, Marija, Vranić, Aleksandra, Janković, Goran, Milojević, Predrag, Stojanović, Ivan, Nenezić, Dragoslav, Ugrešić, Nenad, Kanjuh, Vladimir, Yang, Qin, He, Guo-Wei, "Mechanisms underlying the vasorelaxation of human internal mammary artery induced by (-)-epicatechin" in European Journal of Pharmacology, 762 (2015):306-312,
https://doi.org/10.1016/j.ejphar.2015.05.066 . .

TY  - CONF
AU  - Novaković, Aleksandra
AU  - Marinko, Marija
AU  - Milojević, Predrag
AU  - Babić, Milan
AU  - Stojanović, Ivan
AU  - Jović, Miomir
AU  - Nenezić, Dragoslav
AU  - Ugrešić, Nenad
AU  - Yang, Qin
AU  - He, Guo-Wei
PY  - 2012
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/1728
PB  - Lippincott Williams & Wilkins, Philadelphia
C3  - Circulation
T1  - Relaxation of arterial graft induced by nicorandil
VL  - 125
IS  - 19
SP  - e184
EP  - e184
DO  - 10.1161/CIR.0b013e31824fcdb3
UR  - https://hdl.handle.net/21.15107/rcub_farfar_1728
ER  - 

@conference{
author = "Novaković, Aleksandra and Marinko, Marija and Milojević, Predrag and Babić, Milan and Stojanović, Ivan and Jović, Miomir and Nenezić, Dragoslav and Ugrešić, Nenad and Yang, Qin and He, Guo-Wei",
year = "2012",
publisher = "Lippincott Williams & Wilkins, Philadelphia",
journal = "Circulation",
title = "Relaxation of arterial graft induced by nicorandil",
volume = "125",
number = "19",
pages = "e184-e184",
doi = "10.1161/CIR.0b013e31824fcdb3",
url = "https://hdl.handle.net/21.15107/rcub_farfar_1728"
}

Novaković, A., Marinko, M., Milojević, P., Babić, M., Stojanović, I., Jović, M., Nenezić, D., Ugrešić, N., Yang, Q.,& He, G.. (2012). Relaxation of arterial graft induced by nicorandil. in Circulation
Lippincott Williams & Wilkins, Philadelphia., 125(19), e184-e184.
https://doi.org/10.1161/CIR.0b013e31824fcdb3
https://hdl.handle.net/21.15107/rcub_farfar_1728

Novaković A, Marinko M, Milojević P, Babić M, Stojanović I, Jović M, Nenezić D, Ugrešić N, Yang Q, He G. Relaxation of arterial graft induced by nicorandil. in Circulation. 2012;125(19):e184-e184.
doi:10.1161/CIR.0b013e31824fcdb3
https://hdl.handle.net/21.15107/rcub_farfar_1728 .

Novaković, Aleksandra, Marinko, Marija, Milojević, Predrag, Babić, Milan, Stojanović, Ivan, Jović, Miomir, Nenezić, Dragoslav, Ugrešić, Nenad, Yang, Qin, He, Guo-Wei, "Relaxation of arterial graft induced by nicorandil" in Circulation, 125, no. 19 (2012):e184-e184,
https://doi.org/10.1161/CIR.0b013e31824fcdb3 .,
https://hdl.handle.net/21.15107/rcub_farfar_1728 .

TY  - CONF
AU  - Novaković, Aleksandra
AU  - Pavlović, M.
AU  - Vranić, Aleksandra
AU  - Milojević, Predrag
AU  - Stojanović, Ivan
AU  - Jović, M.
AU  - Nenezić, Dragoslav
AU  - Ugrešić, Nenad
AU  - Yang, Qin
AU  - He, Guo-Wei
PY  - 2012
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/1702
PB  - Oxford Univ Press, Oxford
C3  - Cardiovascular Research
T1  - Different potassium channels are involved in relaxation of arterial graft induced by nicorandil
VL  - 93
DO  - 10.1093/cvr/cvr332
UR  - https://hdl.handle.net/21.15107/rcub_farfar_1702
ER  - 

@conference{
author = "Novaković, Aleksandra and Pavlović, M. and Vranić, Aleksandra and Milojević, Predrag and Stojanović, Ivan and Jović, M. and Nenezić, Dragoslav and Ugrešić, Nenad and Yang, Qin and He, Guo-Wei",
year = "2012",
publisher = "Oxford Univ Press, Oxford",
journal = "Cardiovascular Research",
title = "Different potassium channels are involved in relaxation of arterial graft induced by nicorandil",
volume = "93",
doi = "10.1093/cvr/cvr332",
url = "https://hdl.handle.net/21.15107/rcub_farfar_1702"
}

Novaković, A., Pavlović, M., Vranić, A., Milojević, P., Stojanović, I., Jović, M., Nenezić, D., Ugrešić, N., Yang, Q.,& He, G.. (2012). Different potassium channels are involved in relaxation of arterial graft induced by nicorandil. in Cardiovascular Research
Oxford Univ Press, Oxford., 93.
https://doi.org/10.1093/cvr/cvr332
https://hdl.handle.net/21.15107/rcub_farfar_1702

Novaković A, Pavlović M, Vranić A, Milojević P, Stojanović I, Jović M, Nenezić D, Ugrešić N, Yang Q, He G. Different potassium channels are involved in relaxation of arterial graft induced by nicorandil. in Cardiovascular Research. 2012;93.
doi:10.1093/cvr/cvr332
https://hdl.handle.net/21.15107/rcub_farfar_1702 .

Novaković, Aleksandra, Pavlović, M., Vranić, Aleksandra, Milojević, Predrag, Stojanović, Ivan, Jović, M., Nenezić, Dragoslav, Ugrešić, Nenad, Yang, Qin, He, Guo-Wei, "Different potassium channels are involved in relaxation of arterial graft induced by nicorandil" in Cardiovascular Research, 93 (2012),
https://doi.org/10.1093/cvr/cvr332 .,
https://hdl.handle.net/21.15107/rcub_farfar_1702 .

TY  - JOUR
AU  - Novaković, Aleksandra
AU  - Pavlović, Marija
AU  - Milojević, Predrag
AU  - Stojanović, Ivan
AU  - Nenezić, Dragoslav
AU  - Jović, Miomir
AU  - Ugrešić, Nenad
AU  - Kanjuh, Vladimir
AU  - Yang, Qin
AU  - He, Guo-Wei
PY  - 2012
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/1731
AB  - The ATP-sensitive K+ channels opener (KATPCO), P1075 [N-cyano-N'-(1,1-dimethylpropyl)-N?-3-pyridylguanidine], has been shown to cause relaxation of various isolated animal and human blood vessels by opening of vascular smooth muscle ATP-sensitive K+ (KATP) channels. In addition to the well-known effect on the opening of KATP channels, it has been reported that vasorelaxation induced by some of the KATPCOs includes some other K+ channel subtypes. Given that there is still no information on other types of K+ channels possibly involved in the mechanism of relaxation induced by P1075, this study was designed to examine the effects of P1075 on the rat renal artery with endothelium and with denuded endothelium and to define the contribution of different K+ channel subtypes in the P1075 action on this blood vessel. Our results show that P1075 induced a concentration-dependent relaxation of rat renal artery rings pre-contracted by phenylephrine. Glibenclamide, a selective KATP channels inhibitor, partly antagonized the relaxation of rat renal artery induced by P1075. Tetraethylammonium (TEA), a non-selective inhibitor of Ca2+-activated K+ channels, as well as iberiotoxin, a most selective blocker of large-conductance Ca2+-activated K+ (BKCa) channels, did not abolish the effect of P1075 on rat renal artery. In contrast, a non-selective blocker of voltage-gated K+ (KV) channels, 4-aminopyridine (4-AP), as well as margatoxin, a potent inhibitor of KV1.3 channels, caused partial inhibition of the P1075-induced relaxation of rat renal artery. In addition, in this study, P1075 relaxed contractions induced by 20 similar to mM K+, but had no effect on contractions induced by 80 similar to mM K+. Our results showed that P1075 induced strong endothelium-independent relaxation of rat renal artery. It seems that KATP, 4-AP- and margatoxin-sensitive K+ channels located in vascular smooth muscle mediated the relaxation of rat renal artery induced by P1075.
PB  - Wiley, Hoboken
T2  - Basic & Clinical Pharmacology & Toxicology
T1  - Different Potassium Channels are Involved in Relaxation of Rat Renal Artery Induced by P1075
VL  - 111
IS  - 1
SP  - 24
EP  - 30
DO  - 10.1111/j.1742-7843.2011.00855.x
ER  - 

@article{
author = "Novaković, Aleksandra and Pavlović, Marija and Milojević, Predrag and Stojanović, Ivan and Nenezić, Dragoslav and Jović, Miomir and Ugrešić, Nenad and Kanjuh, Vladimir and Yang, Qin and He, Guo-Wei",
year = "2012",
abstract = "The ATP-sensitive K+ channels opener (KATPCO), P1075 [N-cyano-N'-(1,1-dimethylpropyl)-N?-3-pyridylguanidine], has been shown to cause relaxation of various isolated animal and human blood vessels by opening of vascular smooth muscle ATP-sensitive K+ (KATP) channels. In addition to the well-known effect on the opening of KATP channels, it has been reported that vasorelaxation induced by some of the KATPCOs includes some other K+ channel subtypes. Given that there is still no information on other types of K+ channels possibly involved in the mechanism of relaxation induced by P1075, this study was designed to examine the effects of P1075 on the rat renal artery with endothelium and with denuded endothelium and to define the contribution of different K+ channel subtypes in the P1075 action on this blood vessel. Our results show that P1075 induced a concentration-dependent relaxation of rat renal artery rings pre-contracted by phenylephrine. Glibenclamide, a selective KATP channels inhibitor, partly antagonized the relaxation of rat renal artery induced by P1075. Tetraethylammonium (TEA), a non-selective inhibitor of Ca2+-activated K+ channels, as well as iberiotoxin, a most selective blocker of large-conductance Ca2+-activated K+ (BKCa) channels, did not abolish the effect of P1075 on rat renal artery. In contrast, a non-selective blocker of voltage-gated K+ (KV) channels, 4-aminopyridine (4-AP), as well as margatoxin, a potent inhibitor of KV1.3 channels, caused partial inhibition of the P1075-induced relaxation of rat renal artery. In addition, in this study, P1075 relaxed contractions induced by 20 similar to mM K+, but had no effect on contractions induced by 80 similar to mM K+. Our results showed that P1075 induced strong endothelium-independent relaxation of rat renal artery. It seems that KATP, 4-AP- and margatoxin-sensitive K+ channels located in vascular smooth muscle mediated the relaxation of rat renal artery induced by P1075.",
publisher = "Wiley, Hoboken",
journal = "Basic & Clinical Pharmacology & Toxicology",
title = "Different Potassium Channels are Involved in Relaxation of Rat Renal Artery Induced by P1075",
volume = "111",
number = "1",
pages = "24-30",
doi = "10.1111/j.1742-7843.2011.00855.x"
}

Novaković, A., Pavlović, M., Milojević, P., Stojanović, I., Nenezić, D., Jović, M., Ugrešić, N., Kanjuh, V., Yang, Q.,& He, G.. (2012). Different Potassium Channels are Involved in Relaxation of Rat Renal Artery Induced by P1075. in Basic & Clinical Pharmacology & Toxicology
Wiley, Hoboken., 111(1), 24-30.
https://doi.org/10.1111/j.1742-7843.2011.00855.x

Novaković A, Pavlović M, Milojević P, Stojanović I, Nenezić D, Jović M, Ugrešić N, Kanjuh V, Yang Q, He G. Different Potassium Channels are Involved in Relaxation of Rat Renal Artery Induced by P1075. in Basic & Clinical Pharmacology & Toxicology. 2012;111(1):24-30.
doi:10.1111/j.1742-7843.2011.00855.x .

Novaković, Aleksandra, Pavlović, Marija, Milojević, Predrag, Stojanović, Ivan, Nenezić, Dragoslav, Jović, Miomir, Ugrešić, Nenad, Kanjuh, Vladimir, Yang, Qin, He, Guo-Wei, "Different Potassium Channels are Involved in Relaxation of Rat Renal Artery Induced by P1075" in Basic & Clinical Pharmacology & Toxicology, 111, no. 1 (2012):24-30,
https://doi.org/10.1111/j.1742-7843.2011.00855.x . .

TY  - JOUR
AU  - Gao, Ge
AU  - Bai, Xiao-Yan
AU  - Xuan, Chao
AU  - Liu, Xiao-Cheng
AU  - Jing, Wen-Bin
AU  - Novaković, Aleksandra
AU  - Yang, Qin
AU  - He, Guo-Wei
PY  - 2012
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/1680
AB  - Background and Aims. Intracellular calcium regulation in endothelial cells depends on transient receptor potential channels (TRPs). Canonical TRPs (TRPCs) are now recognized as the most important Ca2+-permeable cation channels in vascular endothelium and TRPC3 channel is reported to play a role in vasodilation in animal vessels. However, little is known about the role of TRPCs in human arteries. We therefore tested the hypothesis that TRPCs play a role in human arteries. Methods. Cumulative concentration-relaxation curves to acetylcholine (-11 to -4.5 log M) were established in the human internal mammary artery (IMA) rings (n = 42) taken from 28 patients undergoing coronary artery bypass grafting in precontraction induced by U46619 (-8 log M) in the absence or presence of SKF96365 (10 mu mol/L) or Pyr3 (3 mu mol/L). Protein expressions of TRPC3 were determined by Western blot and immunohistochemistry staining. Results. The maximal relaxation induced by acetylcholine was significantly attenuated by the nonspecific cation channels inhibitor, SKF96365 (48.2 +/- 3.7 vs. 66.0 +/- 0.9% in control, p  lt  0.01) or the selective TRPC3 blocker, Pyr3 (58.4 +/- 2.3% vs. 67.7 +/- 1.1% in control, p  lt  0.01). Protein expression of TRPC3 was detected in human 1MA. Conclusions. TRPC3 exists and plays a role in the acetylcholine-induced endothelium-dependent relaxation in the human IMA. This study suggests that TRPC3 may be a potential new target in endothelial protection in patients with endothelial dysfunction such as in patients with coronary artery disease in order to improve the long-term patency of the grafting vessels.
PB  - Elsevier Science Inc, New York
T2  - Archives of Medical Research
T1  - Role of TRPC3 Channel in Human Internal Mammary Artery
VL  - 43
IS  - 6
SP  - 431
EP  - 437
DO  - 10.1016/j.arcmed.2012.08.010
ER  - 

@article{
author = "Gao, Ge and Bai, Xiao-Yan and Xuan, Chao and Liu, Xiao-Cheng and Jing, Wen-Bin and Novaković, Aleksandra and Yang, Qin and He, Guo-Wei",
year = "2012",
abstract = "Background and Aims. Intracellular calcium regulation in endothelial cells depends on transient receptor potential channels (TRPs). Canonical TRPs (TRPCs) are now recognized as the most important Ca2+-permeable cation channels in vascular endothelium and TRPC3 channel is reported to play a role in vasodilation in animal vessels. However, little is known about the role of TRPCs in human arteries. We therefore tested the hypothesis that TRPCs play a role in human arteries. Methods. Cumulative concentration-relaxation curves to acetylcholine (-11 to -4.5 log M) were established in the human internal mammary artery (IMA) rings (n = 42) taken from 28 patients undergoing coronary artery bypass grafting in precontraction induced by U46619 (-8 log M) in the absence or presence of SKF96365 (10 mu mol/L) or Pyr3 (3 mu mol/L). Protein expressions of TRPC3 were determined by Western blot and immunohistochemistry staining. Results. The maximal relaxation induced by acetylcholine was significantly attenuated by the nonspecific cation channels inhibitor, SKF96365 (48.2 +/- 3.7 vs. 66.0 +/- 0.9% in control, p  lt  0.01) or the selective TRPC3 blocker, Pyr3 (58.4 +/- 2.3% vs. 67.7 +/- 1.1% in control, p  lt  0.01). Protein expression of TRPC3 was detected in human 1MA. Conclusions. TRPC3 exists and plays a role in the acetylcholine-induced endothelium-dependent relaxation in the human IMA. This study suggests that TRPC3 may be a potential new target in endothelial protection in patients with endothelial dysfunction such as in patients with coronary artery disease in order to improve the long-term patency of the grafting vessels.",
publisher = "Elsevier Science Inc, New York",
journal = "Archives of Medical Research",
title = "Role of TRPC3 Channel in Human Internal Mammary Artery",
volume = "43",
number = "6",
pages = "431-437",
doi = "10.1016/j.arcmed.2012.08.010"
}

Gao, G., Bai, X., Xuan, C., Liu, X., Jing, W., Novaković, A., Yang, Q.,& He, G.. (2012). Role of TRPC3 Channel in Human Internal Mammary Artery. in Archives of Medical Research
Elsevier Science Inc, New York., 43(6), 431-437.
https://doi.org/10.1016/j.arcmed.2012.08.010

Gao G, Bai X, Xuan C, Liu X, Jing W, Novaković A, Yang Q, He G. Role of TRPC3 Channel in Human Internal Mammary Artery. in Archives of Medical Research. 2012;43(6):431-437.
doi:10.1016/j.arcmed.2012.08.010 .

Gao, Ge, Bai, Xiao-Yan, Xuan, Chao, Liu, Xiao-Cheng, Jing, Wen-Bin, Novaković, Aleksandra, Yang, Qin, He, Guo-Wei, "Role of TRPC3 Channel in Human Internal Mammary Artery" in Archives of Medical Research, 43, no. 6 (2012):431-437,
https://doi.org/10.1016/j.arcmed.2012.08.010 . .