Post-excitatory depression in thoracic sympathetic efferent neural traffic during a cardiogenic hypertensive chemoreflex.

Abstract

Serotonin injected in the left atrium activates a cardiogenic hypertensive chemoreflex in dogs. To elucidate patterns of the neural traffic, records were obtained from thoracic sympathetic efferent nerves (either the anterior ansa of the left stellate ganglion or the T4 input to the left stellate) in 8 anesthetized dogs with chest open. Serotonin (200 micrograms, left atrium) caused a massive sympathetic discharge during the hypertension and bracardia characteristic of the chemoreflex. Following the initial sympathetic discharge, there was a consistent post-excitatory depression of neural traffic, to a level significantly less than control discharge (two-tailed p less than .05). This post-excitatory depression began 11 +/- 5.4 (S.D.) seconds after injection of serotonin and 6.6 +/- 5.3 seconds after the peak neural discharge. It lasted 140 +/- 94 seconds, being maximal initially with gradual recovery. Complete block of the hypertension by the combined administration of phentolamine, propranolol, and nitroglycerin failed to abolish the efferent neural events, including post-excitatory depression, in all but one dog. We conclude that post-excitatory depression in thoracic sympathetic efferent neural traffic cannot be mediated exclusively through the secondary engagement of a baroreceptor mechanism and that it most likely is an integral part of the cardiogenic hypertensive chemoreflex.