Abstract

The effect of cocaine, phenoxybenzamine and phentolamine on the catecholamine output from spleen and adrenal medulla was studied.

Splenic nerves were stimulated at frequencies of 10 and 30/sec for a total of 200 stimuli and the blood samples from splenic vein were assayed for norepinephrine. Results are expressed as output of norepinephrine (ng) per stimulus. At 10/sec the amount of norepinephrine was just enough to make an assay possible (0.25 ng/stimulus) while at 30/sec the output was about 4 to 5 times greater (0.67 ng/stimulus) than at 10/sec. Cocaine caused only a slight increment of norepinephrine output at lower frequency while at higher frequency the pattern of output remained the same. Both phenoxybenzamine and phentolamine increased the transmitter output at lower frequency by about 5 times and outputs at lower and higher frequencies were nearly equal. Phenoxybenzamine also caused increase in the background pressor activity of plasma samples.

Splanchnic nerve to the adrenal medulla was stimulated at frequencies of 2, 5, 10, 20 and 30/sec for a total of 300 stimuli, the blood samples were collected from adrenolumbar vein and assayed for total catecholamines. Output of pressor amines was a function of the frequency of nerve stimulation. Cocaine and phentolamine did not have any effect. Phenoxybenzamine, however, increased the background pressor activity quite markedly and also enhanced the catecholamine output at different frequencies.

Cocaine potentiates the submaximal contractions of the nictitating membrane of the cat induced by stimulation of the postganglionic fibers of the superior cervical ganglion. Phenoxybenzamine potentiates the relaxation of the colon in response to submaximal stimulation of the lumbar colonic nerves more effectively than cocaine.

Certain current hypotheses concerning the fate of neurally released transmitter are discussed in relation to the data obtained in the present study. Our present results are in agreement with the hypothesis that adrenergic alpha receptors are involved in the inactivation of the neurally released transmitter from spleen, as originally proposed by Brown and Gillespie (1957).