The changes of the expression of 2-type small conductance-Ca- activating-K (SK2) channel protein in hypertensive rat myocardium.
10.12047/j.cjap.5712.2019.081
- Author:
Wen-Fei ZHANG
1
;
Chang-Zhen YANG
1
;
Peng-Cheng HU
1
;
Hao CHEN
1
;
Yue XI
1
;
Hong-Kun FAN
2
;
Qian ZHANG
2
;
Chun YANG
2
Author Information
1. Clinical College of Zhengzhou University, Zhengzhou 450000.
2. Department of Physiology and Neurobiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou 450000, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Hypertension;
metabolism;
Male;
Myocardium;
metabolism;
Protein-Serine-Threonine Kinases;
metabolism;
Random Allocation;
Rats;
Rats, Sprague-Dawley
- From:
Chinese Journal of Applied Physiology
2019;35(4):381-384
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the expression of 2-type small conductance-Ca-activating-K (SK2) channel protein in hypertensive rat myocardial cells.
METHODS:Twelve healthy adult male SD rats were randomly divided into control group (n=5) and experimental group (n=7). The rats of experimental group were injected intraperitoneally with N'-nitro-L-arginine (L-NNA 15 mg/(kg·d))while the rats of control group were injected intraperitoneally with isometrical normal saline(15 ml/(kg·d )). The body weight, blood pressure and electrocardiogram of the rats were measured every week. After 4 weeks, the rats were sacrificed to obtain hearts, and the expression of SK2 channel protein in myocardium was detected by Western blot.
RESULTS:After 4 weeks of administration, compared with the control group, the blood pressure in the experimental group was significantly elevated (P＜0.05), QRS duration and R-R interval were prolonged, and the expressions of SK2 channel in the atrial and ventricular tissue of the experimental group were significantly higher than those in the control group (1.12±0.18,1.64±0.26, P ＜ 0.05).
CONCLUSION:The expressions of atrial and ventricular SK2 pathway are increased in hypertensive model rats. It may be one of the mechanism leading to arrhythmias in hypertensive model rats and can provide new ideas and strategies for the treatment and prognosis of hypertensive diseases.
