β-estradiol activates BK(Ca) in mesenteric artery smooth muscle cells of post-menopause women.
- Author:
Jun CHENG
1
;
Xiao-Rong ZENG
;
Peng-Yun LI
;
Ting-Ting LU
;
Xiao-Qiu TAN
;
Jing WEN
;
Yan YANG
Author Information
1. Department of Electrophysiology, Luzhou Medical College, Luzhou, China.
- Publication Type:Journal Article
- MeSH:
Aged;
Estradiol;
analogs & derivatives;
pharmacology;
Female;
Humans;
Hypertension;
physiopathology;
Large-Conductance Calcium-Activated Potassium Channels;
agonists;
metabolism;
physiology;
Mesenteric Arteries;
metabolism;
physiology;
Middle Aged;
Muscle, Smooth, Vascular;
cytology;
metabolism;
physiology;
Patch-Clamp Techniques;
Postmenopause;
physiology;
Receptors, Estrogen;
antagonists & inhibitors
- From:
Acta Physiologica Sinica
2012;64(2):121-128
- CountryChina
- Language:Chinese
-
Abstract:
The aim of the present study was to study the effect of β-estradiol (β-E(2)) on the large-conductance Ca(2+)-activated potassium (BK(Ca)) channel in mesenteric artery smooth muscle cells (SMCs). The mesenteric arteries were obtained from post-menopause female patients with abdominal surgery, and the SMCs were isolated from the arteries using an enzymatic disassociation. According to the sources, the SMCs were divided into non-hypertension (NH) and essential hypertension (EH) groups. Single channel patch clamp technique was used to investigate the effect of β-E(2) and ICI 182780 (a specific blocker of estrogen receptor) on BK(Ca) in the SMCs. The results showed the opening of BK(Ca) in the SMCs was voltage and calcium dependent, and could be blocked by IbTX. β-E(2) (100 μmol/L) significantly increased open probability (Po) of BK(Ca) in both NH and EH groups. After β-E(2) treatment, NH group showed higher Po of BK(Ca) compared with EH group. ICI 182780 could inhibit the activating effect of β-E(2) on BK(Ca) in no matter NH or EH groups. These results suggest β-E(2) activates BK(Ca) in mesenteric artery SMCs from post-menopause women via estrogen receptor, but hypertension may decline the activating effect of β-E(2) on BK(Ca).