Faculty Collaboration Database

Chemoreceptor involvement in cortisol responses to hypoxia in ventilated dogs. J Appl Physiol Respir Environ Exerc Physiol 1982 Apr;52(4):1092-6

Date

04/01/1982

Pubmed ID

7085410

DOI

10.1152/jappl.1982.52.4.1092

Scopus ID

2-s2.0-0019961604 (requires institutional sign-in at Scopus site)   12 Citations

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, paralyzed, 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.

Author List

Raff H, Tzankoff SP, Fitzgerald RS

Author

Hershel Raff PhD Professor in the Academic Affairs department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Adrenal Cortex
Animals
Arteries
Blood Pressure
Carbon Monoxide
Chemoreceptor Cells
Dogs
Hydrocortisone
Hydrogen-Ion Concentration
Hypoxia
Male
Oxygen
Partial Pressure
Respiration