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心脏醛固酮生成与心室重构。

Cardiac aldosterone production and ventricular remodeling.

作者信息

Delcayre C, Silvestre J S, Garnier A, Oubenaissa A, Cailmail S, Tatara E, Swynghedauw B, Robert V

机构信息

INSERM U127, Hôpital Lariboisière, IFR Circulation, Université Denis Diderot, Paris, France.

出版信息

Kidney Int. 2000 Apr;57(4):1346-51. doi: 10.1046/j.1523-1755.2000.00973.x.

DOI:10.1046/j.1523-1755.2000.00973.x
PMID:10760065
Abstract

An intracardiac production of aldosterone has been recently reported in rat. This production is increased both acutely and chronically by angiotensin II, observations suggesting that the heart contains a steroidogenic system that is regulated similarly to the adrenal one. Cardiac production of aldosterone is small compared with that of the adrenal, raising the question of its function in normal conditions. Moreover, the regulation of this synthesis in pathophysiologic states remains unknown. In an analysis of the effects of a one-month myocardial infarction (MI) on the cardiac steroidogenic system, it was observed that aldosterone-synthase mRNA and the aldosterone concentration were increased by 2- and 3.5-fold, respectively, in the noninfarcted part of the rat left ventricle. MI also induced a 1. 9-fold increase in the cardiac angiotensin II level. Losartan prevented these changes, and the MI-induced collagen deposition in noninfarcted area of the left ventricle was reduced by 1.6- and 2. 5-fold by both spironolactone and losartan treatments, respectively. Thus, these observations indicate that MI is associated with tissue-specific activation of myocardial aldosterone synthesis. This activation is mediated by cardiac angiotensin II via the angiotensin II type 1 (AT1) receptor, and the resultant increase of intracardiac aldosterone level may be involved in post-MI ventricular remodeling.

摘要

最近有报道称大鼠心脏内可产生醛固酮。血管紧张素II可使醛固酮的急性和慢性生成均增加,这些观察结果提示心脏含有一个类固醇生成系统,其调节方式与肾上腺的类固醇生成系统类似。与肾上腺相比,心脏产生的醛固酮量较少,这就引出了其在正常情况下功能的问题。此外,在病理生理状态下该合成的调节机制仍不清楚。在一项关于为期一个月的心肌梗死(MI)对心脏类固醇生成系统影响的分析中,观察到在大鼠左心室的非梗死部分醛固酮合酶mRNA和醛固酮浓度分别增加了2倍和3.5倍。MI还使心脏血管紧张素II水平升高了1.9倍。氯沙坦可阻止这些变化,螺内酯和氯沙坦治疗分别使MI诱导的左心室非梗死区域的胶原沉积减少了1.6倍和2.5倍。因此,这些观察结果表明MI与心肌醛固酮合成的组织特异性激活有关。这种激活是由心脏血管紧张素II通过1型血管紧张素II(AT1)受体介导的,心脏内醛固酮水平的升高可能参与了MI后的心室重构。

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