Attenuation of hypertension, cardiomyocyte hypertrophy, and myocardial fibrosis by beta-adrenoceptor blockers in rats under long-term blockade of nitric oxide synthesis

dc.creatorPacca, SRMC
dc.creatorde Azevedo, AP
dc.creatorDe Oliveira, CF
dc.creatorDe Luca, IMS
dc.creatorDe Nucci, G
dc.creatorAntunes, E
dc.date2002
dc.dateFEB
dc.date2014-11-17T04:57:47Z
dc.date2015-11-26T16:38:32Z
dc.date2014-11-17T04:57:47Z
dc.date2015-11-26T16:38:32Z
dc.date.accessioned2018-03-28T23:21:55Z
dc.date.available2018-03-28T23:21:55Z
dc.identifierJournal Of Cardiovascular Pharmacology. Lippincott Williams & Wilkins, v. 39, n. 2, n. 201, n. 207, 2002.
dc.identifier0160-2446
dc.identifierWOS:000173401000006
dc.identifier10.1097/00005344-200202000-00006
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/55166
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/55166
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/55166
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1272273
dc.descriptionThe 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.
dc.description39
dc.description2
dc.description201
dc.description207
dc.languageen
dc.publisherLippincott Williams & Wilkins
dc.publisherPhiladelphia
dc.publisherEUA
dc.relationJournal Of Cardiovascular Pharmacology
dc.relationJ. Cardiovasc. Pharmacol.
dc.rightsfechado
dc.sourceWeb of Science
dc.subjectatenolol
dc.subjectN-omega-nitro-L-arginine methyl ester
dc.subjectmyocardial infarction
dc.subjectnitric oxide synthase inhibitors
dc.subjectpropranolol
dc.subjectLeft-ventricular Hypertrophy
dc.subjectAntihypertensive Therapy
dc.subjectChronic Inhibition
dc.subjectSynthase Inhibition
dc.subjectBlood-pressure
dc.subjectAtenolol
dc.subjectModel
dc.subjectRelaxation
dc.subjectNebivolol
dc.subjectIschemia
dc.titleAttenuation of hypertension, cardiomyocyte hypertrophy, and myocardial fibrosis by beta-adrenoceptor blockers in rats under long-term blockade of nitric oxide synthesis
dc.typeArtículos de revistas


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