Downregulated transient outward potassium channel protein Kv4.2 and Kv4.3 expression in PVN contributes to sympathoexcitation in rats with chronic heart failure
10.3969/j.issn.1000-4718.2016.03.022
- VernacularTitle:慢性心衰大鼠下丘脑室旁核瞬时外向钾通道蛋白Kv4.2和 Kv4.3低表达促进肾交感神经兴奋性
- Author:
Liuyi MA
;
Yujie YIN
;
Geng WEI
;
Hongrong LI
;
Junfang ZHANG
;
Huan LIU
;
Zhenhua JIA
- Publication Type:Journal Article
- Keywords:
Chronic heart failure;
Sympathetic nervous;
Hypothalamic paraventricular nucleus;
Ransient out-ward potassium channel protein
- From:
Chinese Journal of Pathophysiology
2016;32(3):522-526,533
- CountryChina
- Language:Chinese
-
Abstract:
[ ABSTRACT] AIM:To investigate the transient outward potassium channel protein expression in paraventricular nucleus (PVN) and its contribution to renal sympathetic nerve activity (RSNA) in rats with chronic heart failure (CHF). METHODS:A rat model of CHF was prepared by acute myocardial infarction that was induced by ligation of the left ante -rior descending coronary artery .Four weeks after heart failure , echocardiogram was applied to identify the CHF model and plasma norepinephrine (NE), serum NH2-terminal pro-brain natriuretic peptide (NT-proBNP) were detected by ELISA. The expression of ransient outward potassium channel proteins Kv 4.2 and Kv4.3 at mRNA and protein levels was deter-mined by real-time PCR and Western blot .The mean arterial pressure ( MAP) , heart rate ( HR) and RSNA were measured in anesthetized rats with PVN microinjection of potassium channel blockers 4-AP.RESULTS:In CHF group , the rat car-diac function and Kv4.2 and Kv4.3 expression in PVN were obviously lower while plasma NE and serum NT-proBNP were obviously higher than those in sham group .Microinjection of 4-AP into PVN induced an increase in MAP , HR and RSNA in both sham and CHF rats , while the CHF rats exhibited smaller responses to 4-AP than sham-operated rats .CONCLU-SION:Downregulation of Kv4.2 and Kv4.3 expression in the PVN may be a potential mechanism for sympathoexciation in the rats with chronic heart failure .
