OBSERVATIONS ON THE INITIAL HYPERTENSIVE RESPONSE TO RESERPINE

¹ Department of Pharmacology, University of Michigan, Ann Arbor

The unanesthetized dog paralyzed with gallamine or decamethonium shows an initial marked rise in arterial blood pressure within 5 to 20 minutes following the intravenous administration of large doses (1 mgm./kgm.) of reserpine acetate or phosphate. Considerable variability exists in the magnitude and onset of this pressor response. Such a pressor response may last from one-half hour after reserpine administration to as long as 1 to 2 hours. Such a pressor response is seldom present in unanesthetized cats and rabbits. A minor initial pressor response to the administration of reserpine is also found in dogs anesthetized with pentobarbital or alpha chloralose, but it is quantitatively reduced.

Ganglionic blockade enhances the initial pressor response to reserpine in both anesthetized and unanesthetized dogs paralyzed with neuromuscular blocking agents.

Pentobarbital anesthesia reduces, and Dibenzyline abolishes the initial pressor response to reserpine.

The initial pressor response to reserpine does not appear to be due to circulating serotonin since the administration of large doses of cocaine block the pressor response to exogenously administered serotonin but do not prevent the pressor response due to reserpine.

Bilateral adrenalectomy does not prevent the initial pressor response to reserpine.

Reserpine produces a diphasic EEG response in unanesthetized dogs paralyzed with decamethonium. During the initial hypertension EEG arousal with intervals of slow wave activity was observed. During the hypotensive phase of reserpine action the slow wave activity was observed more frequently than in control animals. Invariably sensory stimuli were effective in producing arousal.