Document Detail


Effects of poststroke losartan versus captopril treatment on myogenic and endothelial function in the cerebrovasculature of SHRsp.
MedLine Citation:
PMID:  17379826     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND AND PURPOSE: We assessed the ability of poststroke captopril and losartan treatment to reverse myogenic and endothelial dysfunction in the middle cerebral arteries of Kyoto-Wistar stroke-prone spontaneously hypertensive rats (SHRsp) that developed intracerebral hemorrhagic stroke. METHODS: SHRsp were sampled before and after stroke development and after up to 37 days of captopril (50 mg/kg per day) or losartan (35 mg/kg per day) treatment initiated after stroke. Pressure-dependent constriction to a 100-mm Hg pressure step, constriction to nitric oxide synthase inhibition (100 micromol/L N(omega)-nitro-l-arginine methyl ester), and endothelium-dependent vasodilation to bradykinin (1.6 micromol/L), 2-f-LIGRLO-NH(2) (1 micromol/L, a protease-activated receptor-2 agonist), and A23187 (2 micromol/L) were evaluated in middle cerebral arteries at 100 mm Hg with a pressure myograph. RESULTS: Middle cerebral arteries from SHRsp with stroke could not constrict to pressure or nitric oxide synthase inhibition, lacked the ability to vasodilate to bradykinin, and exhibited attenuated dilation and vasomotion in response to A23187. Vasodilation to 2-f-LIGRLO-NH(2) was unaltered. The aforementioned cerebrovascular alterations were reversed after 31 days of poststroke losartan but not of captopril treatment in the absence of an antihypertensive effect. Captopril treatment restored middle cerebral artery constriction to pressure, NOS inhibition, and bradykinin vasodilation temporarily after 7 to 18 days of treatment, after which function deteriorated to a level observed in SHRsp at stroke. CONCLUSIONS: Aspects of poststroke cerebrovascular dysfunction, which likely play an important role in altering and modulating cerebral blood flow autoregulation, can be reversed in SHRsp more effectively after stroke development by blocking angiotensin II type 1 receptors as opposed to lowering angiotensin II levels.
Authors:
John S Smeda; John J McGuire
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-03-22
Journal Detail:
Title:  Stroke; a journal of cerebral circulation     Volume:  38     ISSN:  1524-4628     ISO Abbreviation:  Stroke     Publication Date:  2007 May 
Date Detail:
Created Date:  2007-04-24     Completed Date:  2007-05-15     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0235266     Medline TA:  Stroke     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1590-6     Citation Subset:  IM    
Affiliation:
Division of Basic Medical Sciences, Memorial University, Health Science Center, St John's, Newfoundland, Canada. jsmeda@mun.ca
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MeSH Terms
Descriptor/Qualifier:
Animals
Antihypertensive Agents / pharmacology*
Captopril / pharmacology*
Cerebrovascular Circulation / drug effects*
Endothelium, Vascular / drug effects
Losartan / pharmacology*
Male
Rats
Rats, Inbred Strains
Receptor, Angiotensin, Type 1 / drug effects
Stroke / complications,  drug therapy*
Vascular Diseases / drug therapy,  etiology
Vasodilation / drug effects
Chemical
Reg. No./Substance:
0/Antihypertensive Agents; 0/Receptor, Angiotensin, Type 1; 114798-26-4/Losartan; 62571-86-2/Captopril

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


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