Inhibitory effect of 18β-glycyrrhetinic acid on KCl- and PE-induced constriction of rat renal interlobar artery in vitro.
- Author:
Wen ZHANG
1
;
Ke-Tao MA
;
Yang WANG
;
Jun-Qiang SI
;
Li LI
Author Information
1. Department of Physiology/Key Laboratory of Education Ministry of Xinjiang Endemic and Ethnic Diseases, Medical College of Shihezi University, Shihezi 832002, China. Lily7588@163.com.
- Publication Type:Journal Article
- MeSH:
Animals;
Arteries;
drug effects;
physiopathology;
Constriction;
Gap Junctions;
Glycyrrhetinic Acid;
analogs & derivatives;
pharmacology;
In Vitro Techniques;
Myocytes, Smooth Muscle;
cytology;
Patch-Clamp Techniques;
Rats;
Rats, Wistar
- From:
Acta Physiologica Sinica
2014;66(2):195-202
- CountryChina
- Language:Chinese
-
Abstract:
The aim of the present study is to investigate the effect of 18β-glycyrrhetinic acid (18β-GA) on KCl- and PE-induced constriction of rat renal interlobar artery (RIA). Pressure myograph system was used to observe the constriction induced by KCl and PE (endothelial independent vasoconstrictor) in acutely separated RIA of Wistar rats with or without 18β-GA pretreatment. Whole-cell patch clamp recordings were used to observe the effect of 18β-GA on membrane input capacitance (C(input)), membrane input conductance (G(input)) or membrane input resistance (R(input)) of smooth muscle cells embedded in arteriole segment. The results showed that both KCl (30-100 mmol/L) and PE (0.1-30 μmol/L) induced contraction of RIA in a concentration-dependent way. After pretreatment with 18β-GA (100 μmol/L), KCl- or PE-induced constriction of RIA was significantly decreased. After application of 18β-GA (100 μmol/L), the C(input), G(input) and R(input) of the in situ smooth muscle cells were very close to those of dispersed single smooth muscle cells. These results suggest 18β-GA inhibits the contraction induced by KCl and PE, and the underlying mechanism may involve the inhibitory effect of 18β-GA on gap junction.
