Trevethan CS

Language: Spanish
References: 10
Page: 216-219
PDF size: 50.54 Kb.

ABSTRACT

Studies performed in the last five years have led to the knowledge of new mechanisms by which the hypertensive process produces hypertrophy and cardiac fibrosis, at the same time, favoring development of the atheroesclerotic plaque. The Renin-Angiotensin-Aldosterone axis is relevant by involved in the physiophatology of these alterations, not only by producing hyperplasia and hypertrophy of vascular smooth muscle cells or by increasing protein and DNA syntheses, mediated by Angiotensin II (by itself a potent Growth factor) but also through inflammatory processes exerted upon the vascular smooth muscle cells. These alterations (hypertrophy, fibrosis, inflammation, and destabilization of the atherosclerotic plaque) can now be counteracted by blocking the Angiotensin-Converting enzyme or its AT1 receptors with the consequent improvement in ventricular diastolic functions.

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