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Endothelium-dependent vasorelaxant effect of procyanidin B2 on human internal mammary artery

Authorized Users Only
2017
Authors
Novaković, Aleksandra
Marinko, Marija
Janković, Goran
Stojanović, Ivan
Milojević, Predrag
Nenezić, Dragoslav
Kanjuh, Vladimir
Yang, Qin
He, Guo-Wei
Article (Published version)
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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.

Keywords:
Procyanidin B2 / Human internal mammary artery / Vasorelaxation / K+ channels / Intracellular calcium / Endothelium
Source:
European Journal of Pharmacology, 2017, 807, 75-81
Publisher:
  • Elsevier Science BV, Amsterdam
Funding / projects:
  • Investigation of the Effect and Mechanism of Action of Different Vasodilator Substances on the Human Bypass Grafts (RS-175088)

DOI: 10.1016/j.ejphar.2017.04.015

ISSN: 0014-2999

PubMed: 28414054

WoS: 000403520300009

Scopus: 2-s2.0-85017480494
[ Google Scholar ]
25
18
URI
https://farfar.pharmacy.bg.ac.rs/handle/123456789/2972
Collections
  • Radovi istraživača / Researchers’ publications
Institution/Community
Pharmacy
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 . .

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