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

Academic Article

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 chests open. Serotonin (200 μg, left atrium) caused a massive sympathetic discharge during the hypertension and bradycardia 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≤.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 postexcitatory 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. © 1982 Dr. Dietrich Steinkopff Verlag.
  • Published In

    Digital Object Identifier (doi)

    Author List

  • Kilbourne EM; Hageman GR; James TN; Urthaler F
  • Start Page

  • 423
  • End Page

  • 430
  • Volume

  • 77
  • Issue

  • 4