| Role of cardiac renin-angiotensin system in the development of pressure-overload left ventricular hypertrophy in rats with abdominal aortic constriction. | |
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MedLine Citation:
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PMID: 8717433 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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D S Reddy; M Singh; S Ghosh; N K Ganguly |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Molecular and cellular biochemistry Volume: 155 ISSN: 0300-8177 ISO Abbreviation: Mol. Cell. Biochem. Publication Date: 1996 Feb |
Date Detail:
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Created Date: 1997-01-14 Completed Date: 1997-01-14 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0364456 Medline TA: Mol Cell Biochem Country: NETHERLANDS |
Other Details:
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Languages: eng Pagination: 1-11 Citation Subset: IM |
Affiliation:
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Department of Pharmacology, Panjab University, Chandigarh, India. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Angiotensin-Converting Enzyme Inhibitors
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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:
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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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