Fibrosis and renin-angiotensin-aldosterone system activity. Reality and future prospects
https://doi.org/10.18705/1607-419X-2012-18-5-449-458
Abstract
Myocardial fibrosis plays a key role in the pathogenesis of cardiovascular diseases. Renin-angiotensin-aldosterone system (RAAS) is the key regulator of vascular tone, potassium and water homeostasis, and response to the tissue damage. The effects of angiotesin II are mediated by 1 type angiotensin II receptors, together with angiotensin-converting enzyme, forming the «classical regulation axis» of RAAS. At chronic high cardiac afterload the genes of procollagen and collagen synthesis are overexpressed leading to the increased production of collagen, fibrosis and myocardial hypertrophy. Both hemodynamic and non-hemodynamic factors affect fibrosis development. RAAS blockers are suggested to have antifibrotic activity. There is a strong evidence of losartan efficiency that can be, at least, partly mediated by antifibrotic activity.
About the Authors
O. M. Drapkina
I.M. Sechenov First Moscow State Medical University
Russian Federation
Russian Federation
Yu. S. Drapkina
I.M. Sechenov First Moscow State Medical University
Russian Federation
Russian Federation
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Review
For citations:
Drapkina O.M., Drapkina Yu.S. Fibrosis and renin-angiotensin-aldosterone system activity. Reality and future prospects. "Arterial’naya Gipertenziya" ("Arterial Hypertension"). 2012;18(5):449-458. (In Russ.) https://doi.org/10.18705/1607-419X-2012-18-5-449-458
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