Document Detail


Role of angiotensin II in early cardiovascular growth and vascular amplifier development in spontaneously hypertensive rats.
MedLine Citation:
PMID:  9321741     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: To examine the role played by angiotensin II (AII) in the development of prehypertensive vascular hypertrophy in the spontaneously hypertensive rat (SHR) and to determine whether normalization of prehypertensive vascular hypertrophy attenuates the development of hypertension. DESIGN: Male SHR and Wistar-Kyoto (WKY) rats were treated from age 10 days until age 6 weeks with perindopril, an angiotensin converting enzyme (ACE) inhibitor, or with losartan, a type 1 AII receptor antagonist. METHODS: At termination of treatment, or 8 weeks after cessation of treatment, vascular growth was assessed by measurement of hindquarter resistance properties and of the medial cross-sectional area of first-order mesenteric arteries. The growth of the heart was assessed by measurement of the left ventricle:body weight ratio. RESULTS: Perindopril and losartan treatment of SHR and WKY rats led to a heterogeneous response in the vasculature, resulting in a reduction in perfusion pressures at maximum dilatation and constriction in the hindquarter vasculature but no significant change in medial cross-sectional area of small mesenteric arteries. Neither perindopril nor losartan treatment affected the growth of the left ventricle in the SHR. After the cessation of treatment the development of hypertension in the losartan- and perindopril-treated SHR did not differ from that in controls. CONCLUSION: These results suggest that AII, acting via angiotensin type 1 receptors, plays an important role in determining the early post-natal reactivity of the hindquarter vasculature but not the medial cross-sectional area of the mesenteric vasculature, which implies that different growth regulatory mechanisms are operating in the two vascular beds. The lack of effect in some vascular beds, together with the lack of effect on the heart, may account for the absence of a persistent effect on the blood pressure.
Authors:
M J Black; P Kanellakis; A Bobik
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of hypertension     Volume:  15     ISSN:  0263-6352     ISO Abbreviation:  J. Hypertens.     Publication Date:  1997 Sep 
Date Detail:
Created Date:  1998-01-13     Completed Date:  1998-01-13     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8306882     Medline TA:  J Hypertens     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  945-54     Citation Subset:  IM    
Affiliation:
Baker Medical Research Institute, Victoria, Australia.
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MeSH Terms
Descriptor/Qualifier:
Angiotensin II / antagonists & inhibitors,  physiology*
Angiotensin-Converting Enzyme Inhibitors / pharmacology,  therapeutic use
Animals
Animals, Newborn
Antihypertensive Agents / pharmacology,  therapeutic use
Body Weight / drug effects
Cardiomegaly / prevention & control
Cardiovascular System / drug effects,  pathology*
Hypertension / etiology*,  pathology,  prevention & control
Hypertrophy / prevention & control*
Indoles / pharmacology,  therapeutic use
Kidney / pathology
Losartan / pharmacology,  therapeutic use
Male
Mesenteric Arteries / anatomy & histology,  drug effects
Organ Size / drug effects
Papaverine / pharmacology
Perindopril
Rats
Rats, Inbred SHR
Rats, Inbred WKY
Time Factors
Vascular Resistance / drug effects*
Chemical
Reg. No./Substance:
0/Angiotensin-Converting Enzyme Inhibitors; 0/Antihypertensive Agents; 0/Indoles; 11128-99-7/Angiotensin II; 114798-26-4/Losartan; 58-74-2/Papaverine; 82834-16-0/Perindopril

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


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