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Isoliquiritigenin‐induced vasodilation by activating large‐conductance Ca 2+ ‐activated K + channels in mouse mesenteric arteries
Author(s) -
Ye Yang,
Gao Mengru,
Feng Lei,
Feng Bainian,
Ma Xin
Publication year - 2019
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.13156
Subject(s) - iberiotoxin , myograph , vasodilation , mesenteric arteries , phenylephrine , medicine , vascular smooth muscle , chemistry , apamin , potassium channel , endocrinology , hyperpolarization (physics) , endothelium derived hyperpolarizing factor , artery , charybdotoxin , blood pressure , stereochemistry , smooth muscle , nuclear magnetic resonance spectroscopy
Abstract Isoliquiritigenin ( ISL ) is a flavonoid substance with a chalcone structure, which exerts anti‐tumour, anti‐oxidation and anti‐inflammatory activity. The large‐conductance calcium‐activated potassium channel ( BK C a ) is an important potassium channel with negative feedback regulation on the vascular smooth muscle cells ( VSMC s) membrane. The activation of BK C a channel causes the hyperpolarization of VSMC s. It plays an important role in relaxation of blood vessels. Previous studies have shown that ISL causes the relaxation of the aorta and the basilar artery of the rat. However, there have not been studies on regulation of ISL in mesenteric arteries. To examine whether ISL causes the relaxation of the mesenteric artery of mice, we recorded vasodilation of mouse mesenteric arterial rings with a myograph. After contraction of arterial rings with phenylephrine, we added ISL to the arterial rings and measured its relaxation effect. To further examine which channel was involved in this relaxation effect, we tested the effects of ISL on endothelium‐dependent and endothelium‐independent vasodilation. Then we used BK C a channel blockers tetraethylammonium and iberiotoxin, to detect whether the BK C a channel is involved in ISL ‐induced vasodilation. Mesenteric arterial smooth muscle cells were isolated by enzyme digestion. Bis‐(1, 3‐dibutylbarbituric acid) trimethine oxonol staining was used to measure membrane potential of mesenteric arterial smooth muscle cells. We identified a vasodilation effect caused by ISL on mouse mesenteric arterial rings pre‐contracted by phenylephrine in a concentration‐dependent manner, with an EC 50 of 13.71 ± 1.1 μmol/L. The vasodilation effect of ISL is endothelium‐independent. K + channel inhibitors tetraethylammonium and iberiotoxin reduced the vasodilation induced by ISL which suggested the involvement of BK C a channel.