Document Detail

Renin-angiotensin system and minoxidil-induced cardiac hypertrophy in rats.
MedLine Citation:
PMID:  8238566     Owner:  NLM     Status:  MEDLINE    
Besides cardiac volume overload, cardiac sympathetic activity and the renin-angiotensin system (RAS) are activated by arterial vasodilators such as minoxidil. To evaluate the possible involvement of the RAS in the development of minoxidil-induced cardiac hypertrophy, we assessed in normotensive rats minoxidil-induced changes in cardiac and plasma renin activity (PRA) and the potential of chronic treatment with the angiotensin-converting enzyme (ACE) inhibitor enalapril and the nonpeptide angiotensin II receptor blocker losartan to prevent minoxidil-induced cardiac hypertrophy. PRA increased in parallel with the increase in cardiac filling pressures and development of cardiac hypertrophy, whereas the increase in cardiac renin activity was delayed as compared with these changes. Losartan did not decrease left ventricular end-diastolic pressure (LVEDP) but prevented the remodeling of the heart by minoxidil. In contrast, enalapril nearly normalized LVEDP but did not affect the hypertrophic response of the heart. The losartan data indicate that the RAS is involved in the minoxidil-induced cardiac hypertrophy either directly (e.g., by mediating the hypertrophic response of the heart to cardiac volume overload) or indirectly (e.g., by potentiating cardiac sympathetic activity). The ineffectiveness of enalapril has no obvious explanation but may possibly indicate ineffective blockade of angiotensin II formation in the heart in this model.
M Ruzicka; F H Leenen
Related Documents :
24952036 - Safety and effectiveness evidence of sam? junctional tourniquet to control inguinal hem...
6399316 - Effects of brain renin-angiotensin on cardiovascular function and saline intake in awak...
9690046 - The role of endothelin in hypertension.
6989756 - Mechanism of enhanced blood pressure rise after reclipping following removal of a renal...
22207116 - Cardiotrophin-1 plasma levels are increased in patients with diastolic heart failure.
10212346 - Office versus ambulatory heart rate in the prediction of the cardiovascular risk.
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The American journal of physiology     Volume:  265     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1993 Nov 
Date Detail:
Created Date:  1993-12-20     Completed Date:  1993-12-20     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  H1551-6     Citation Subset:  IM    
Hypertension Unit, University of Ottawa Heart Institute, Ontario, Canada.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Angiotensin II / antagonists & inhibitors
Biphenyl Compounds / pharmacology*
Blood Pressure / drug effects
Cardiomegaly / chemically induced,  physiopathology*
Enalapril / pharmacology*
Heart / drug effects,  physiology,  physiopathology*
Hemodynamics / drug effects*
Imidazoles / pharmacology*
Minoxidil / pharmacology*,  toxicity
Rats, Wistar
Renin / blood
Renin-Angiotensin System* / drug effects
Tetrazoles / pharmacology*
Ventricular Function, Left / drug effects
Reg. No./Substance:
0/Biphenyl Compounds; 0/Imidazoles; 0/Tetrazoles; 11128-99-7/Angiotensin II; 114798-26-4/Losartan; 38304-91-5/Minoxidil; 75847-73-3/Enalapril; EC

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

Previous Document:  Interaction of hypokalemia and ventricular dilatation in isolated rabbit hearts.
Next Document:  Effect of hypoxemia on the cardiovascular response to intracranial hypertension in postnatal lambs.