© 2000 by European Society of Cardiology
Copyright © 2000, European Society of Cardiology
Renin–angiotensin–aldosterone system and myocardial fibrosis
Center of Internal Medicine, Division of Cardiology, Philipps University of Marburg, Marburg, Germany
* Tel.: +49-6421-286-4980; fax: +49-6421-286-8954 brilla@t-online.de
Received 30 March 2000; accepted 5 April 2000
| The first 150 words of the full text of this article appear below. |
See article by Bishop et al. [26] (pages 57–67) in this issue.
During the past decade, evidence has been provided that the circulating and local renin–angiotensin–aldosterone systems (RAAS) promote the development of myocardial fibrosis in hypertensive heart disease and chronic heart failure [1,2] including in vitro experiments using adult rat cardiac fibroblasts where both angiotensin II (AngII) [3–5] and aldosterone [3] stimulate collagen synthesis in a dose-dependent manner while AngII additionally suppresses the activity of matrix metalloproteinase 1, the key enzyme of interstitial collagen degradation [3], that synergistically leads to progressive collagen accumulation within the myocardial interstitium. This could be proved in in vivo studies in renovascular hypertension [1], with chronic administration of aldosterone [1,6,7], or in the spontaneously hypertensive rat (SHR) model of genetic hypertension [8–12] where a local cardiac AngII generating system is operative [13]. Therefore, the physiological role of RAAS on the development
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