Document Detail

Control of blood pressure and end-organ damage in maturing salt-loaded stroke-prone spontaneously hypertensive rats by oral angiotensin II receptor blockade.
MedLine Citation:
PMID:  8382237     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: To study the effects of renin-angiotensin system blockade by a novel non-peptide angiotensin II receptor antagonist, losartan, on development of hypertension and acceleration of end-organ damage in salt-loaded stroke-prone spontaneously hypertensive rats (SHRSP). DESIGN AND METHODS: One hundred and eighty-one male SHRSP were fed a 4% sodium diet from 6 to 18 weeks of age. Seventy-eight SHRSP were treated orally with losartan, 30 mg/kg per day. One hundred and three rats constituted untreated controls. Blood pressure, plasma renin activity (PRA), renal function and end-organ damage were monitored during the transition to malignant hypertension. RESULTS: Losartan prevented a blood pressure rise during the first 4 weeks of salt loading. Thereafter, blood pressure rose slowly in losartan-treated rats; however, at each time-point studied blood pressure was significantly lower in losartan-treated rats than in control rats. Losartan treatment increased PRA during the first 4 weeks, but this effect was not sustained. Thereafter, PRA decreased to control (week 0) levels. In contrast, 2 weeks after high-sodium feeding started, untreated SHRSP failed to suppress PRA appropriately; thereafter, PRA rose significantly. Losartan affected renal pathophysiology by blunting the decline in glomerular filtration rate, controlling proteinuria and preventing or delaying the appearance of malignant nephrosclerosis. Losartan treatment significantly increased survival and completely prevented cerebrovascular infarcts. CONCLUSIONS: The results indicate that angiotensin II blockade markedly reduces both hypertension and end-organ damage in chronically salt-loaded SHRSP and that the renin-angiotensin system may play an important role in the development of hypertensive cardiovascular disease in SHRSP.
M J Camargo; N von Lutterotti; W G Campbell; M S Pecker; G D James; P B Timmermans; J H Laragh
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of hypertension     Volume:  11     ISSN:  0263-6352     ISO Abbreviation:  J. Hypertens.     Publication Date:  1993 Jan 
Date Detail:
Created Date:  1993-03-22     Completed Date:  1993-03-22     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  8306882     Medline TA:  J Hypertens     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  31-40     Citation Subset:  IM    
Department of Medicine, Cornell University Medical College, New York, NY 10021.
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MeSH Terms
Angiotensin II / antagonists & inhibitors*
Biphenyl Compounds / pharmacology*
Blood Proteins / metabolism
Body Weight / drug effects
Brain / pathology
Chlorides / blood,  urine
Creatinine / blood
Diuresis / drug effects
Hypertension / complications,  drug therapy*,  metabolism
Imidazoles / pharmacology*
Kidney / pathology
Myocardium / pathology
Organ Size
Osmolar Concentration
Potassium / blood,  urine
Proteinuria / metabolism
Rats, Inbred SHR
Renin / blood
Renin-Angiotensin System / drug effects
Sodium / blood,  urine
Tetrazoles / pharmacology*
Grant Support
Reg. No./Substance:
0/Biphenyl Compounds; 0/Blood Proteins; 0/Chlorides; 0/Imidazoles; 0/Tetrazoles; 11128-99-7/Angiotensin II; 114798-26-4/Losartan; 60-27-5/Creatinine; 7440-09-7/Potassium; 7440-23-5/Sodium; EC

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

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