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Abstract
Classically, the production of glucocorticoids by the adrenal gland is thought to
be controlled exclusively by adrenocorticotropic hormone (ACTH). However, there are
several examples in stressed humans and animals of increased plasma glucocorticoids
in the absence of increased plasma ACTH, suggesting that an additional, non-ACTH mechanism(s)
may contribute to the control of glucocorticoid production. The present studies were
designed to determine the role of the thoracic splanchnic nerve in controlling plasma
corticosterone levels in response to chronic water deprivation in rats, a model previously
reported to demonstrate dissociations between plasma corticosterone and ACTH. Briefly,
rats underwent right unilateral adrenalectomy and left thoracic splanchnic nerve transection
or sham transection. After recovery, rats were water deprived for 48 h or given free
access to water, and then sacrificed for collection of plasma and adrenal glands.
Water deprivation resulted in consistent, robust increases in plasma corticosterone
that were attenuated by splanchnic nerve transection, in the absence of changes in
post-dehydration plasma ACTH. Adrenal content of steroidogenic acute regulatory factor
(StAR) and cyclic AMP (cAMP) were increased after dehydration; splanchnic nerve transection
decreased post-dehydration adrenal cAMP, but not StAR. Splanchnic nerve transection
also attenuated plasma corticosterone responses to submaximal doses of ACTH in dexamethasone-blocked,
dehydrated rats, suggesting a decreased adrenal sensitivity to ACTH. Collectively,
the present results demonstrate that the thoracic splanchnic nerve normally augments
the adrenal corticosterone response to dehydration stress by increasing adrenal sensitivity
to ACTH, and this augmentation is associated with elevations in adrenal cAMP content.
These data support the hypothesis that the splanchnic innervation of the adrenal gland
represents an additional physiological mechanism to control stress-induced adrenal
cortical responses in vivo.