Mechanisms of Inhibition of Heart Rate by Phenylephrine

H P HE RATIONALE for using the vasocon••strictor agent phenylephrine to revert paroxysmal auricular tachycardia was that it would be expected to elicit cardioinhibitory reflexes from the rise in pressure in the carotid sinuses and aortic arch." However, Keys and Violante suggested the possibility that phenylephrine "produces a primary bradycardia by inhibition of the sinoauricular node and this is relatively independent of blood pressure reflexes over the vagus nerve." They interpreted results of a later study as indicating that phenylephrine "stimulates effectors of both sympathetic and parasyinpathetic nervous systems—the action of the drug is partly adrenergic and partly cholinergic." A dual basis for the cardioinhibitory action of phenylephrine, as postulated by Keys and Violante, has been referred to in more recent articles as though it is an established fact.' Since the hypothesis of a dual action of phenylephrine seems logical in view of the prominent cardioinhibitoiy action of the compound, the studies reported here were designed to determine if phenylephrine has an effect on heart rate in some way other than the action elicited reflexly from pressoreceptors.