Emodin-induced increase in expression of β1 subunit of BKCa channel mediates relaxation of cerebral basilar artery in spontaneously hypertensive rats.
- Author:
Chuan-Lin ZHANG
1
;
Li-Na CONG
;
Rui WANG
;
Yang WANG
;
Ke-Tao MA
;
Lei ZHAO
;
Jun-Qiang SI
;
Li LI
Author Information
1. Electrophysiological Laboratory, Laboratory of Xinjiang Endemic and Ethnic Diseases, Shihezi University Medical College, Shihezi 832002, China. lily7588@163.com.
- Publication Type:Journal Article
- MeSH:
Animals;
Basilar Artery;
cytology;
Blood Pressure;
Emodin;
pharmacology;
Large-Conductance Calcium-Activated Potassium Channel alpha Subunits;
metabolism;
Myocytes, Smooth Muscle;
metabolism;
Patch-Clamp Techniques;
Rats;
Rats, Inbred SHR;
Rats, Wistar;
Vasodilation;
Vasodilator Agents;
pharmacology
- From:
Acta Physiologica Sinica
2014;66(3):289-294
- CountryChina
- Language:Chinese
-
Abstract:
The purposes of this study were to investigate the effect of emodin on expression of BKCa channel β1 subunit in basilar artery smooth muscle cells (BASMCs) and electrophysiological characteristics of vascular smooth muscle cells in spontaneously hypertensive rats (SHR). Tail artery pressure measurement instrument was used to measure the change of SHR systolic blood pressure before and after emodin intervention. Single vascular smooth muscle cell was electrically recorded by whole-cell patch-clamp technique. Immunohistochemistry and Western blotting were used to study the distribution and expression of the BKCa channel β1 subunit. The results showed that emodin decreased blood pressure of SHR from (223 ± 16) mmHg to (127 ± 12) mmHg (P < 0.01). There was no difference of blood pressure between emodin-treated SHR and Wistar rats. Emodin significantly increased outward currents of smooth muscle cells in SHR (P < 0.05), and this effect could be reversed by specific inhibitor of BKCa channel, IbTX. Emodin also up-regulated BKCa channel β1 subunit expression in BASMCs. These results suggest that emodin relaxes cerebral basilar artery by enhancing BKCa current via increasing β1 subunit expression in BASMCs.
