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  - 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 . .