Open AccessFibrosis and renin-angiotensin-aldosterone system activity. Reality and future prospects
Author(s) -
О. М. Драпкина,
Yu. S. Drapkina
Publication year - 2012
Publication title -
arterialʹnaâ gipertenziâ
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.126
H-Index - 5
eISSN - 2411-8524
pISSN - 1607-419X
DOI - 10.18705/1607-419x-2012-18-5-449-458
Subject(s) - renin–angiotensin system , medicine , losartan , aldosterone , fibrosis , angiotensin ii , endocrinology , homeostasis , pathogenesis , afterload , myocardial fibrosis , cardiac fibrosis , hemodynamics , receptor , blood pressure
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.