Document Detail


Is there an internal cardiac renin-angiotensin system?
MedLine Citation:
PMID:  8983664     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The beneficial effects of angiotensin converting enzyme (ACE) inhibitors in heart failure appear to be independent, at least in part, of their effect on blood pressure. The existence of a local cardiac renin angiotensin system is often suggested as an explanation. It has been known for some time that a substantial proportion of arterially delivered angiotensin I is converted to angiotensin II by ACE of the coronary vascular endothelium. The levels of angiotensin II in cardiac tissue are several times the levels of angiotensin II in circulating blood. Recent evidence suggests that most of the angiotensin II in the heart is not derived from angiotensin I in the circulation, and that most of the angiotensin I in cardiac tissue is generated in the tissue itself. On the other hand, renin mRNA levels are very low or undetectable in the normal heart. In addition, studies on the effects of bilateral nephrectomy on the cardiac tissue levels of renin, angiotensin I, and angiotensin II in pigs have indicated that cardiac renin originates from the kidney and that cardiac generation of angiotensin I and angiotensin II depends on renin from the kidney. Intracardiac synthesis of renin may occur under pathological conditions and during fetal development. The fact that angiotensins are generated by the heart raises the possibility of local mechanisms to regulate the concentrations of these peptides at certain tissue sites. For example, preliminary evidence suggests that binding of renin to cardiac membranes is a mechanism by which renin is taken up by the heart. A specific renin binding protein has been identified in cardiac tissue. Cardiac ACE levels may also influence local angiotensin II formation and are, in part, determined by the so called insertion/deletion ACE gene polymorphism. More detailed knowledge on the site of angiotensin generation and on its regulation will improve our understanding of the role of the renin-angiotensin system in cardiac function, hypertrophy, and postinfarction remodelling.
Authors:
A H Danser; M A Schalekamp
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Heart (British Cardiac Society)     Volume:  76     ISSN:  1355-6037     ISO Abbreviation:  Heart     Publication Date:  1996 Nov 
Date Detail:
Created Date:  1997-01-09     Completed Date:  1997-01-09     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  9602087     Medline TA:  Heart     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  28-32     Citation Subset:  AIM; IM    
Affiliation:
Cardiovasculair Onderzoeksinstituut Erasmus, Universiteit Rotterdam (COEUR), The Netherlands.
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MeSH Terms
Descriptor/Qualifier:
Angiotensin I / metabolism
Angiotensin II / metabolism,  physiology
Animals
Humans
Kidney / metabolism
Myocardium / metabolism*
Peptidyl-Dipeptidase A / metabolism
Rats
Renin / metabolism
Renin-Angiotensin System / physiology*
Sheep
Swine
Transcription, Genetic
Chemical
Reg. No./Substance:
11128-99-7/Angiotensin II; 9041-90-1/Angiotensin I; EC 3.4.15.1/Peptidyl-Dipeptidase A; EC 3.4.23.15/Renin
Comments/Corrections

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