Chemoreceptor involvement in cortisol responses to hypoxia in ventilated dogs

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Abstract
Changes in cortisol secretion rate (CSR) in response to hypoxic hypoxia (HH) and to CO hypoxia (COH) were assessed in mongrel dogs that had intact chemoreceptors (INT), surgically deafferented carotid bodies (LCBD) 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; in CBD and SAD animals, the CSR was attenuated but not eliminated. COH, which does not stimulate the carotid body, caused the submaximal increase in CSR regardless of chemoreceptor status. The carotid bodies are the principal chemoreceptor influence on CSR during HH. There is a nonchemoreceptor-mediated increase in CSR during hypoxia.