Changes of cardiac aldosterone and mineralocorticoid receptor in rats with chronic heart failure induced by isoproterenol
10.3760/cma.j.issn.0254-9026.2011.02.026
- VernacularTitle:异丙肾上腺素诱导慢性心力衰竭大鼠心肌醛固酮及其核受体的变化
- Author:
Xiaoqin ZHU
;
Huashan HONG
;
Yuanhong LI
;
Qiong JIANG
;
Lianglong CHEN
- Publication Type:Journal Article
- Keywords:
Isoproterenol;
Heart failure,congestive;
Aldosterone
- From:
Chinese Journal of Geriatrics
2011;30(2):168-171
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the changes of cardiac aldosterone and mineralocorticoid receptor (MR) in Sprague-dawley (SD) rats with chronic heart failure (CHF) induced by isoproterenol (ISO). Methods The SD rats were randomly divided into CHF group (n=9) and normal control(NC) group (n=10). The experimental CHF group was induced by subcutaneous injection of ISO, and the NC group received same dose injection of sodium chloride. The heart function was evaluated with both echocardiography and hemodynamics. The contents of aldosterone in both plasma and heart were assessed by radioimmunoassay. The expression of MR was measured by Western blot and immunohistochemistry staining. Results Compared with NC group, the heart function was decreased in CHF group, the left ventricular ejection fraction was (38.8%±4.0%) in CHF and(79. 4%±4.6%), in NC group. The maximal rate of increase of ventricular pressure (+dp/dtmax) was (7164.4±502.6) mm Hg(1 mm Hg=0.133 kPa)/s in CHF and (10199.5±462.9) mm Hg/s in NC group (both P＜0. 01 ). The contents of aldosterone both in plasma and heart were higher in CHF group than in NC group [(0.63±0.06)μg/L vs. (0.3±0.07) μg/L, (0.41±0.05) μg/kgvs. (0.08±0.01)μg/kg, both P＜0. 01]. The MR expression was increased in CHF group versus in NC group (P＜0.01). Conclusions The heart function is decreased in rats with CHF induced by ISO, which is similar to dilated cardiomyopathy. The higher levels of aldosterone both in circulation and in heart as and well as MR expression upregulation in heart may play important roles in the pathogenesis of CHF induced by ISO.
