Document Detail

Role of NO and angiotensin II in the early development of endothelial functions impairment and cardiac hypertrophy in deoxycorticosterone acetate-salt hypertension.
MedLine Citation:
PMID:  9923405     Owner:  NLM     Status:  MEDLINE    
This study was designed to investigate the effects of chronic inhibition of NO synthesis as well as chronic angiotensin receptor blockade with losartan in the development of hypertension, on mesenteric arterial bed reactivity as well as on the development of cardiac and kidney hypertrophy in deoxycorticosterone-salt (DOCA) hypertension. Uninephrectomized rats were divided in four experimental groups all receiving saline water to drink and treated or not with losartan over a period of 9 days. Two of these groups were administered DOCA, one of which received also N(G)-nitro-L-arginine-methyl ester (L-NAME) to drink. A third group received only L-NAME, while another group received only saline. Systolic blood pressure was similarly increased in L-NAME, DOCA, DOCA-L-NAME groups. Cardiac and kidney weights were increased in DOCA but significantly reduced in DOCA-L-NAME. Losartan prevented the development of hypertension in all groups and also prevented cardiac and kidney hypertrophy in DOCA. The hyperreactivity of mesenteric arteries to phenylephrine, measured in the presence of indomethacin, was endothelium-dependent in both L-NAME groups but not in DOCA rats. Pretreatment with BQ 123 did not modify these endothelium-dependent responses in L-NAME rats. Chronic losartan prevented endothelium-dependent phenylephrine hyperreactivity only in DOCA, whereas only the removal of the endothelium attenuated the responsiveness in both L-NAME-treated groups. Vasorelaxations to acetylcholine and isoproterenol were attenuated in the three hypertensive groups and were normalized only in DOCA and L-NAME treated with losartan. In summary, in all hypertensive groups, blood pressure was normalized by losartan independently of its effects on endothelial functions. In DOCA, losartan normalized the phenylephrine hyperreactivity through an endothelial-dependent mechanism. However, in L-NAME-treated groups an endothelial-derived contracting factor, other than angiotensin II, endothelin, or vasoconstrictor prostanoids, appears to be activated. Both NO and angiotensin II seem to play a role in the early development of hypertension and organ hypertrophy in DOCA hypertension.
A K-Laflamme; L Oster; R Cardinal; J de Champlain
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Canadian journal of physiology and pharmacology     Volume:  76     ISSN:  0008-4212     ISO Abbreviation:  Can. J. Physiol. Pharmacol.     Publication Date:  1998 Jun 
Date Detail:
Created Date:  1999-04-13     Completed Date:  1999-04-13     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0372712     Medline TA:  Can J Physiol Pharmacol     Country:  CANADA    
Other Details:
Languages:  eng     Pagination:  665-75     Citation Subset:  IM    
Department of physiology, Faculty of Medicine, Université de Montréal, QC, Canada.
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MeSH Terms
Angiotensin II / physiology*
Antihypertensive Agents / pharmacology
Cardiomegaly / etiology,  physiopathology*
Endothelium, Vascular / physiopathology*
Hypertension / chemically induced,  complications,  physiopathology*
Losartan / pharmacology
NG-Nitroarginine Methyl Ester / pharmacology
Nitric Oxide / physiology*
Nitric Oxide Synthase / antagonists & inhibitors
Nitric Oxide Synthase Type III
Organ Size / drug effects
Rats, Sprague-Dawley
Sodium Chloride
Splanchnic Circulation / drug effects
Reg. No./Substance:
0/Antihypertensive Agents; 10102-43-9/Nitric Oxide; 11128-99-7/Angiotensin II; 114798-26-4/Losartan; 50903-99-6/NG-Nitroarginine Methyl Ester; 64-85-7/Desoxycorticosterone; 7647-14-5/Sodium Chloride; EC Oxide Synthase; EC Oxide Synthase Type III; EC protein, rat

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