THE CHEMOCEPTOR STIMULANT ACTION OF SEROTONIN IN DOGS

¹ Research Division of the Cleveland Clinic Foundation and the Frank E. Bunts Educational Institute, Cleveland, Ohio

Serotonin caused pronounced increase in chemoceptor impulse traffic in the carotid sinus nerve when given in amounts of 12 microgm. into the common carotid artery.

By use of a perfusion system permitting chemoceptors to be excluded from the natural circulation, it was found that small doses of serotonin fail to stimulate respiration unless the drug reaches them.

Section of the spinal cord at C₆ and cervical section of the vago-aortic trunks did not eliminate the respiratory response to intravenous serotonin. Subsequent removal of the carotid chemoceptors by section of the sinus nerves did. Much larger doses caused the reappearance of a respiratory response; the mechanism of this residual effect is assumed to be central—it persists after cervical section of the spinal cord with section of the vagus-aortic and sinus nerves.

Chemoceptor stimulation contributes to the pressor response elicited by intravenous injection of serotonin. The response usually became less pressor and more depressor when chemoceptors were removed from the natural circulation.

Serotonin was a more powerful chemoceptor stimulant than lobeline, tryptamine or DMPP. Its action, like that of anoxia, was not blocked by TEAC; the action of DMPP was. TEAC given systemically blocked the arterial pressure response, but not the respiratory response to serotonin chemoceptor stimulation.

This article has been cited by other articles:

				S. R. Chiocchio, A. M. Biscardi, and J. H. Tramezzani 5-Hydroxytryptamine in the Carotid Body of the Cat Science, November 10, 1967; 158(3802): 790 - 791. [Abstract] [PDF]