Propranolol has been shown to possess a specific β-receptor blocking action and, as another pharmacological property, a nonspecific local anesthetic or quinidine-like action. Responses of cardiovascular system to the administration of propranolol alone are not always dependent on β-receptor inhibition and that some of these responses were related to a nonspecific action has been illustrated by experiments using d-isomer that possessed little β-receptor blocking potency; therefore much of the recent analyses concerned the problem of whether the effects exerted upon the cardiovascular system by propranolol was mediated through a specific receptor inhibition or through nonspecific action. In this paper, propranolol intracoronarily injected with coronary artery catheterization produced a transient coronary vasodilation of variable degrees dependent on the dose used, without changes in ECG and blood pressure in closed-chest dogs, and similar observations were obtained by d- or l-isomer. Phenoxybenzamine, an α-adrenergic blocking agent, also exerted a weak dilator action on the coronary vasculature as with propranolol. Experiments were carried out with similar methods in an attempt to verify whether these responses resulted from their blocking action on the adrenergic receptors or not, using reserpinized dogs with the coronary perfusion with “red-cell Tyrode solution”; coronary vasodilation was produced in a degree more pronounced than in non-treated dogs. These results suggest that the dilator action do not result from adrenergic blockade but may arise from their other pharmacological properties.
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