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Downregulated transient outward potassium channel protein Kv4.2 and Kv4.3 expression in PVN contributes to sympathoexcitation in rats with chronic heart failure / 中国病理生理杂志
Chinese Journal of Pathophysiology ; (12): 522-526,533, 2016.
Artigo em Chinês | WPRIM | ID: wpr-603909
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-SIONDownregulation of Kv4.2 and Kv4.3 expression in the PVN may be a potential mechanism for sympathoexciation in the rats with chronic heart failure .

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Pathophysiology Ano de publicação: 2016 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Pathophysiology Ano de publicação: 2016 Tipo de documento: Artigo