Why the study?
Do beta-blockers (propranolol or atenolol) reduce arterial hypertension, cardiomyocyte hypertrophy, and myocardial fibrosis in rats with chronic nitric oxide deficiency?
Do beta-blockers (propranolol or atenolol) reduce arterial hypertension, cardiomyocyte hypertrophy, and myocardial fibrosis in rats with chronic nitric oxide deficiency?
Beta-blockers (propranolol and atenolol) attenuate hypertension, cardiac hypertrophy, and fibrosis induced by chronic nitric oxide deficiency in a rat model.
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.
No takes yet. Share an insight, caveat, or question.
Pacca et al. (2002) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: