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[Restructuring of the collagen network in hypertension: role of the angiotensin-aldosterone system].

UNLABELLED
Myocardial fibrosis as a consequence of systemic hypertension is a determinant factor in alteration of cardiac function. It has been postulated that this fibrous reaction is under the influence of an elevation of blood aldosterone. To gain further insight into the mechanisms that result in an accumulation of cardiac collagen, we used a model of aldosterone-salt-induced hypertension in rat. Uninephrectomized male Wistar rats weighting 200 g were perfused with 0.75 microgram/hr aldosterone and received 1% NaCl + 0.3% KCl in the drinking water for 2 months.


RESULTS
1) Arterial hypertension was evidenced as soon as 15 days and reached 40% at 2 months. 2) The left ventricle (LV) was hypertrophied by 45% at 2 months and its relative content in mRNA coding for the beta-isoform of the myosin heavy chain was increased by 142%. 3) The microscopic examination of hemalun-eosin stained LV showed a number of important foci of proliferating non-muscular cells, of inflammatory aspect. 4) The LV collagen concentration as measured by hydroxyproline assay was not changed whereas an histological study done on Sirius red-stained slides showed that the interstitial and perivascular collagen network was more important in treated rats. 5). The abundance of mRNAs coding for the alpha 1 chain of type I collagen was increased by 60%. Our results suggest that the fibrous response involves a pretranslational regulation of collagen synthesis.