Document Detail

Age-related increase in sensitivity for ischemic ATP breakdown in hypertrophic hearts of SHR normalized by enalapril.
MedLine Citation:
PMID:  8072019     Owner:  NLM     Status:  MEDLINE    
We evaluated, firstly, the sensitivity to cardiac ischemic ATP breakdown during the development of hypertension and cardiac hypertrophy in Spontaneously Hypertensive Rats (SHR) v Wistar Kyoto (WKY) controls, and secondly, the effects of short-term (8 days) and prolonged (3 months) antihypertensive treatment with the angiotensin converting enzyme inhibitor enalapril on hypertrophy and sensitivity to global ischemia. In isolated perfused hearts, ischemia was induced by a stepwise lowering of the perfusion pressure and the appearance of the ATP breakdown products (purines) in the coronary effluent was assessed as a measure of ischemia. Hearts from 2.5- and 4-month-old SHR started to release purines at a higher perfusion pressure than hearts of WKY, associated with a higher maximum concentration in the coronary effluent. This increased ischemic ATP breakdown in 2.5- and 4-month-old SHR could be attributed to a decreased flow at a given perfusion pressure, because of a two-fold increase in coronary vascular resistance (CVR). In contrast, the maximal purine concentration in the coronary effluent in hearts of 7-month-old SHR was reduced compared to the younger SHR and only slightly higher than 7-month-old WKY, despite a persistent increase in CVR. Enalapril normalized the blood pressure, but only prolonged treatment, significantly prevented and regressed cardiac hypertrophy, and reduced CVR. Whereas enalapril did not influence ATP breakdown in WKY, in SHR both short- and long-term treatment normalized it to the pattern observed in WKY. We conclude that during the early phase of cardiac hypertrophy the hearts of SHR become more sensitive to ischemic ATP breakdown solely because of an increase in CVR, whereas during the established hypertrophic phase, the hearts appear to adapt metabolically, resulting in normalized purine release. Enalapril normalized the transient increase in sensitivity to ischemic ATP breakdown during the development of hypertension in SHR, independent of effects on cardiac hypertrophy, apparently by improving coronary flow at low perfusion pressures.
R G Schoemaker; F H Leenen; E Harmsen
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  26     ISSN:  0022-2828     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  1994 May 
Date Detail:
Created Date:  1994-09-29     Completed Date:  1994-09-29     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  649-60     Citation Subset:  IM    
Hypertension Unit, University of Ottawa Heart Institute, Canada.
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MeSH Terms
Adenosine Triphosphate / metabolism*
Aging / metabolism*,  physiology
Blood Pressure / drug effects,  physiology
Enalapril / pharmacology*,  therapeutic use
Hypertension / drug therapy,  metabolism*,  physiopathology
Hypertrophy, Left Ventricular / metabolism*,  physiopathology
Myocardial Ischemia / metabolism*,  physiopathology
Purines / metabolism
Rats, Inbred SHR
Rats, Inbred WKY
Time Factors
Vascular Resistance / drug effects,  physiology
Reg. No./Substance:
0/Purines; 56-65-5/Adenosine Triphosphate; 75847-73-3/Enalapril

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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