Tissue renin-angiotensin systems. Their role in cardiovascular disease

Tools

Item Type:	Review
Title:	Tissue renin-angiotensin systems. Their role in cardiovascular disease
Creators Name:	Lee, M.A., Boehm, M., Paul, M. and Ganten, D.
Abstract:	BACKGROUND: The identification of the components of the renin-angiotensin system (RAS) in various extrarenal tissues suggested the existence of local renin-angiotensin systems with organ-specific functions that may act independently from the plasma RAS. These findings have led to the hypothesis of paracrine-autocrine functions of the RAS, which implies that locally generated angiotensin II mediates effects within one tissue or within one cell. Whereas the circulating endocrine RAS appears to be responsible for acute effects, the tissue RAS seems to participate in more chronic processes such as secondary structural changes and therefore may contribute to the pathogenesis of hypertension as well as other cardiovascular disorders such as cardiac hypertrophy, coronary artery disease, and atherosclerosis. METHODS AND RESULTS: The use of molecular biological techniques has demonstrated that all components of the RAS-renin, angiotensinogen, converting enzyme, and angiotensin receptors-are expressed in several tissues that participate in the regulation of cardiovascular homeostasis. CONCLUSIONS: The therapeutic importance of inhibitors of the RAS, such as converting enzyme inhibitors, is based on their cardioprotective as well as antiproliferative effects and points to a direct involvement of the RAS in the development and preservation of primary hypertension, a pathological condition in which normal or even low plasma renin activity is a common finding. Reversal of cardiovascular structural changes and enhancement of renal sodium excretion by converting enzyme inhibitors are important long-term antihypertensive actions possibly mediated by inhibition of the tissue RAS.
Keywords:	Renin-Angiotensin System, Hypertension, Converting Enzyme Inhibitor, Kidney, Heart, Vasculature, Animals
Source:	Circulation
ISSN:	0009-7322
Publisher:	American Heart Association
Volume:	87
Number:	Suppl IV
Page Range:	7-13
Date:	May 1993
PubMed:	View item in PubMed

Repository Staff Only: item control page