Abstract

Both reserpine and a semisynthetic analogue, syrosingopine (Su 3118), release heart norepinephrine of rabbits in doses that do not release brain norepinephrine or serotonin. Reserpine exerts this selectivity for peripheral norepinephrine over a small dosage range. Syrosingopine is as effective as reserpine in releasing heart norepinephrine, but does not appreciably release brain amines or elicit sedation over a wide range of doses.

Doses of syrosingopine which do not sedate dogs or release appreciable amounts of brain amines reduce the activity of the sympathetic nervous system by depleting norepinephrine at peripheral neurons. The effects of the "chemical sympathectomy" include decreased blood pressure, bradycardia, reduction in the pressor responses to occlusion of carotid arteries and to electrical stimulation of the central end of cut vagus, reversal of pressor responses to TMA, and diminution of pressor response to electrical stimulation of celiac ganglion. In addition the pressor and cardiac accelerating effects of administered norepinephrine are enhanced.

The view is presented that the sedative and hypotensive actions of reserpine and its analogues do not have a common central mechanism but that these compounds apparently exert two distinct and separate actions, one peripheral and the other central.