Chemoreceptor involvement in cortisol responses to hypoxia in ventilated dogs

H. Raff, S. P. Tzankoff, R. S. Fitzgerald

Research output: Contribution to journalArticle

Abstract

Changes in cortisol secretion rate (CSR) in response to hypoxic hypoxia (HH) and to carbon monoxide hypoxia (COH) were assessed in mongrel dogs that had intact chemoreceptors (INT); surgically deafferented carotid bodies (CBD) or aortic bodies (ABD); or both carotid and aortic chemoreceptors denervated (SAD). All dogs were anesthetized, ventilated, and maintained normocapnic. In the INT and ABD groups, CSR responded 'maximally' to HH, whereas in CBD and SAD animals, the CSR was attenuated but not eliminated. COH, which does not stimulate the carotid body, caused a submaximal increase in CSR regardless of chemoreceptor status. It is concluded that 1) the carotid bodies are the principal chemoreceptor influence on CSR during HH and 2) there is a nonchemoreceptor-mediated increase in CSR during hypoxia.

Original languageEnglish (US)
Pages (from-to)1092-1096
Number of pages5
JournalJournal of Applied Physiology Respiratory Environmental and Exercise Physiology
Volume52
Issue number4
DOIs
StatePublished - 1982

ASJC Scopus subject areas

  • Physiology
  • Endocrinology

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