Abstract
Results of a further attempt to determine a basis for the qualitative difference in blood pressure response of the human and the dog to l-phenyl-2-hydrazinopropane are reported. Elimination of arterial pressure level as a factor influencing the circulatory response of the dog to this compound removes the last possibility for a circumstantial basis for the difference. Mechanism studies indicate that the canine pressor response is a neurotropic, sympathetic effect mediated, for the most part, as a direct action on myoneural junction receptor sites with a lesser component of indirect action on these sites related to MAO inhibition or the peripheral release of catecholamines from blood vessel walls. Evidence presented by certain clinical investigators points to either a ganglionic or an adrenergic block as responsible for the human antihypertensive effect.
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