Chemoreceptor involvement in cortisol responses to hypoxia in ventilated dogs.
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.
D000302:Adrenal Cortex / Q000098:blood supply; D000818:Animals; D001158:Arteries; D001794:Blood Pressure; D002248:Carbon Monoxide / Q000494:pharmacology; D002628:Chemoreceptor Cells / Q000502:physiology*; D004285:Dogs; D006854:Hydrocortisone / Q000378:metabolism*; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia / Q000139:chemically induced / Q000378:metabolism*; D008297:Male; D010100:Oxygen / Q000097:blood; D010313:Partial Pressure; D012119:Respiration
D002248:Carbon Monoxide; D010100:Oxygen; D006854:Hydrocortisone