Document Detail


Resistance artery mechanics and composition in angiotensin II-infused rats: effects of aldosterone antagonism.
MedLine Citation:
PMID:  12544451     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Angiotensin (Ang) II stimulates aldosterone production, which may mediate some of the effects of Ang II. OBJECTIVE: To test whether Ang II-induced structural and mechanical changes in resistance arteries may be prevented by the non-selective aldosterone receptor blocker, spironolactone, independently of reduction in blood pressure. METHODS: Male Sprague-Dawley rats received Ang II [120 ng/kg per min subcutaneously (s.c.)] with or without spironolactone or hydralazine (25 mg/kg per day). Two additional groups received aldosterone (750 ng/h s.c.) with or without spironolactone. After 2 weeks, third-order mesenteric arteries were dissected and studied by pressurized myograph. Deposition of collagen type I/III in the vascular wall was evaluated by confocal immunofluorescence microscopy. RESULTS: Ang II increased blood pressure significantly (P <0.01); this was partially prevented by spironolactone (P <0.01) and nearly normalized by hydralazine (P <0.01). Media thickness, media:lumen ratio and media cross-sectional area of mesenteric resistance arteries increased under Ang II or aldosterone (P <0.01) and this was partially prevented by spironolactone (P <0.01), but not by hydralazine. Compared with the control or Ang II + spironolactone groups, rats treated with Ang II with or without hydralazine presented stiffer vessels, with leftward shift of the stress-strain relationship and a raised slope of the incremental elastic modulus-stress relationship (P <0.05). Confocal microscopy demonstrated enhanced deposition of collagen type I/III in the media of arteries from rats infused with Ang II or aldosterone, an effect that was prevented partially by spironolactone but unaffected by hydralazine. CONCLUSION: Ang II-induced vascular alterations in structure, mechanics and composition were partially prevented by spironolactone, independently of blood pressure reduction, providing further evidence that some actions of Ang II on resistance arteries are mediated by aldosterone.
Authors:
Mario Fritsch Neves; Agostino Virdis; Ernesto L Schiffrin
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of hypertension     Volume:  21     ISSN:  0263-6352     ISO Abbreviation:  J. Hypertens.     Publication Date:  2003 Jan 
Date Detail:
Created Date:  2003-01-24     Completed Date:  2003-07-30     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8306882     Medline TA:  J Hypertens     Country:  England    
Other Details:
Languages:  eng     Pagination:  189-98     Citation Subset:  IM    
Affiliation:
Multidisciplinary Research Group on Hypertension, Canadian Institutes of Health Research, Clinical Research Institute of Montreal, 110 Pine Avenue West, Montreal, Quebec, Canada H2W 1R7.
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MeSH Terms
Descriptor/Qualifier:
Aldosterone Antagonists / pharmacology*
Angiotensin II / pharmacology*
Animals
Antihypertensive Agents / pharmacology
Blood Pressure / drug effects
Collagen / metabolism
Hydralazine / pharmacology
Male
Mesenteric Arteries / drug effects*,  pathology,  physiopathology*
Microscopy, Confocal
Rats
Rats, Sprague-Dawley
Renin / blood
Spironolactone / pharmacology*
Vascular Resistance*
Vasodilator Agents / pharmacology
Chemical
Reg. No./Substance:
0/Aldosterone Antagonists; 0/Antihypertensive Agents; 0/Vasodilator Agents; 11128-99-7/Angiotensin II; 52-01-7/Spironolactone; 86-54-4/Hydralazine; 9007-34-5/Collagen; EC 3.4.23.15/Renin

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


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