Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/195049
Type: Artigo de periódico
Title: Attenuation Of Hypertension, Cardiomyocyte Hypertrophy, And Myocardial Fibrosis By Beta-adrenoceptor Blockers In Rats Under Long-term Blockade Of Nitric Oxide Synthesis.
Author: Pacca, Sandra R M C
de Azevedo, Ana Paula
De Oliveira, Claudia F
De Luca, Iara M S
De Nucci, Gilberto
Antunes, Edson
Abstract: The effects of propranolol and atenolol were investigated on arterial hypertension, cardiomyocyte hypertrophy, and ventricular ischaemic lesions induced by an 8-week treatment with the nitric oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME; 20 mg/rat per day) in Wistar rats. Propranolol and atenolol (30 mg/rat per day each) were given in the drinking water concomitantly to L-NAME. Treatment with L-NAME induced marked arterial hypertension and cardiomyocyte hypertrophy, both of which were significantly reduced by propranolol and atenolol. A marked repairing fibrosis was also observed in L-NAME-treated rats and this was significantly attenuated in animals receiving the beta-blockers. In L-NAME group, 33% mortality was observed, whereas all the animals from the other groups survived. Our study demonstrates that propranolol and atenolol reduce arterial hypertension, cardiomyocyte hypertrophy and myocardial fibrosis induced by L-NAME, suggesting that beta-blockers are of beneficial value in treatment of vascular and cardiac alterations caused by chronic nitric oxide deficiency.
Subject: Adrenergic Beta-1 Receptor Antagonists
Adrenergic Beta-antagonists
Animals
Atenolol
Blood Pressure
Body Weight
Enzyme Inhibitors
Fibrosis
Heart
Hypertension
Hypertrophy, Left Ventricular
Male
Myocardium
Ng-nitroarginine Methyl Ester
Nitric Oxide
Nitric Oxide Synthase
Organ Size
Propranolol
Rats
Rats, Wistar
Time Factors
Rights: fechado
Identifier DOI: 
Address: http://www.ncbi.nlm.nih.gov/pubmed/11791005
Date Issue: 2002
Appears in Collections:Unicamp - Artigos e Outros Documentos

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