Document Detail


Role of cardiac renin-angiotensin system in the development of pressure-overload left ventricular hypertrophy in rats with abdominal aortic constriction.
MedLine Citation:
PMID:  8717433     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Possible involvement of cardiac renin-angiotensin system (RAS) in pressure overload induced left ventricular hypertrophy (LVH) was investigated. Rats were subjected to abdominal aortic constriction (AAC) and examined the effects of 4 weeks treatments with an angiotensin converting enzyme (ACE) inhibitor, captopril and a vasodilator, hydralazine on haemodynamics and ventricular RNA, DNA, protein and myosin isoform pattern in sham and hypertrophied rats. AAC increased the mean arterial pressure (MAP) and systolic blood pressure (SBP), and resulted in increased left ventricle/body weight ratio, LV thickness, RNA and protein content, however total DNA was not changed. The expression of fetal isogene, beta-myosin heavy chain (beta-MHC), was markedly enhanced where as alpha-MHC was reduced. High-dose captopril (100 mg/kg p.o.,) significantly prevented the increase in haemodynamics, development of LVH, LV remodeling, increase in total protein, RNA and antithetical expression of myosin isoforms. Hydralazine (15 mg/kg p.o.,), did not modulate hypertrophic changes and low-dose captopril (1.5 mg/kg p.o.,) which has not produced any marked fall in MAP and SBP also modulated favourably the development of LVH and its biochemical markers. Thus, the prevention of the development of LVH and induction of beta-MHC by non-hypotensive doses of captopril may be related to the blockade of intracardiac production of angiotensin II rather than circulating system. These results suggest that cardiac RAS may play an important role in pressure overload induced LVH.
Authors:
D S Reddy; M Singh; S Ghosh; N K Ganguly
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Molecular and cellular biochemistry     Volume:  155     ISSN:  0300-8177     ISO Abbreviation:  Mol. Cell. Biochem.     Publication Date:  1996 Feb 
Date Detail:
Created Date:  1997-01-14     Completed Date:  1997-01-14     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0364456     Medline TA:  Mol Cell Biochem     Country:  NETHERLANDS    
Other Details:
Languages:  eng     Pagination:  1-11     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, Panjab University, Chandigarh, India.
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MeSH Terms
Descriptor/Qualifier:
Angiotensin-Converting Enzyme Inhibitors / pharmacology
Animals
Aorta, Abdominal
Blood Pressure / drug effects
Body Weight / drug effects
Captopril / pharmacology
Carotid Arteries / drug effects,  physiology,  physiopathology
DNA / analysis
Female
Heart / drug effects,  physiology,  physiopathology*
Heart Ventricles
Hemodynamics / drug effects,  physiology*
Hydralazine / pharmacology
Hypertrophy, Left Ventricular / physiopathology*
Myocardium / metabolism
Myosin Heavy Chains / analysis
Organ Size / drug effects
RNA / analysis
Rats
Rats, Inbred Strains
Reference Values
Renin-Angiotensin System* / drug effects
Time Factors
Vasodilator Agents / pharmacology
Chemical
Reg. No./Substance:
0/Angiotensin-Converting Enzyme Inhibitors; 0/Myosin Heavy Chains; 0/Vasodilator Agents; 62571-86-2/Captopril; 63231-63-0/RNA; 86-54-4/Hydralazine; 9007-49-2/DNA

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


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