Propranolol (10 to 30 μg/kg), oxprenolol (trasicor) (5 to 10 μg/kg), and sotalol (10 to 50 μg/kg) evoke an acute and prolonged increase of arterial pressure in normal and nephrectomized rats, while after adrenalectomy the arterial pressure remains unchanged or is reduced. The pressor effect is accompanied by a reduction of heart rate. The dose of the three beta blockers evoking an arterial pressure increase does not antagonize the effect of isopropylnoradrenaline. To block the beta receptors, doses 10 to 100 times higher than those effective on arterial pressure have to be used. The block of the beta receptors is accompanied by an initial fall of the blood pressure and by a significant decrease of the heart rate. The pressor effect of beta blockers is not antagonized but rather is potentiated by phenoxybenzamine and phentolamine. Moreover, in the presence of an alpha receptor blockade, the administration of beta blockers partially restores the response to catecholamines. These results support the hypothesis that the pressor effect evoked by beta receptor blocking agents may be due: (a) to the release of endogenous catecholamines and (b) to the interference by beta blockers with phenoxybenzamine and phentolamine on the alpha receptors.
The effects of .BETA.-blocking agents on mitochondrial function in ischemic myocardium.
