18β-glycyrrhetinic acid inhibits outward current of vascular smooth muscle cells of arterioles.
- Author:
Ke-Tao MA
1
;
Xin-Zhi LI
;
Li LI
;
Zhong-Shuang ZHANG
;
Wen-Yan SHI
;
Jun-Qiang SI
Author Information
1. The Key Laboratory of Xinjiang Endemic and Ethnic Diseases, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Arterioles;
physiology;
Cerebellum;
blood supply;
Female;
Gap Junctions;
physiology;
Glycyrrhetinic Acid;
analogs & derivatives;
pharmacology;
Guinea Pigs;
In Vitro Techniques;
Male;
Membrane Potentials;
drug effects;
Mesenteric Arteries;
cytology;
physiology;
Muscle, Smooth, Vascular;
cytology;
physiology;
Myocytes, Smooth Muscle;
physiology;
Patch-Clamp Techniques;
Potassium Channels, Calcium-Activated;
physiology;
Potassium Channels, Voltage-Gated;
physiology
- From:
Acta Physiologica Sinica
2011;63(6):549-554
- CountryChina
- Language:Chinese
-
Abstract:
The aim of the present study was to investigate the effect of 18β-glycyrrhetinic acid (18βGA) on the membrane current of vascular smooth muscle cells (VSMCs) in arteriole. Guinea pig anterior inferior cerebellar artery (AICA) and mesenteric artery (MA) were isolated, and single VSMCs were harvested using digestion with papain and collagenase IA. Outward currents of the VSMCs were recorded by whole-cell patch clamp technique. Results were shown as below: (1) 1 mmol/L 4-AP and 1 mmol/L TEA both could partially inhibit the whole-cell current of VSMCs in arterioles. (2) 18βGA inhibited the outward current of VSMCs in a concentration-dependent manner. The inhibitory rates of 10, 30 and 100 μmol/L 18βGA on the membrane current of VSMCs (+40 mV) were (25.3 ± 7.1)%, (43.1 ± 10.4)% and (68.4 ± 3.9)% respectively in AICA, and (13.2 ± 5.6)%, (34.2 ± 4.0)% and (59.3 ± 7.3)% respectively in MA. There was no significant difference between the inhibitory effects of 18βGA on AICA and MA. 18βGA also inhibited the outward current of VSMCs in a voltage-dependent manner. 18βGA induced a more pronounced inhibition of the outward current from 0 to +40 mV, especially at +40 mV. (3) With the pretreatment of 10 mmol/L TEA, the inhibitory effect of 18βGA on the membrane current of VSMCs was significantly abolished. These results suggest that the outward current of VSMCs in arterioles is mediated by voltage-dependent K(+) channels (K(v)) and big conductance calcium-activated K(+) channels (BK(Ca)), which can be inhibited by 18βGA in concentration- and voltage-dependent way.
