Dehydration, but not vasopressin infusion, enhances the adrenocortical responses of sheep to corticotropin-releasing hormone or restraint

Abstract

Two experiments were carried out using adult castrated sheep prepared with jugular vein catheters. In Experiment 1, sheep (N=8) were injected iv with saline vehicle, vehicle + 15 or 30 \g=m\g oCRH, or subjected to 120 min mild physical stress (restraint), following a 48 h period during which water was freely available or withheld. Blood samples were taken for 30 min before and 120 min after oCRH injection, and before and during restraint, and the plasma analysed for AVP and cortisol content. Levels of AVP increased by over 500% after dehydration, but were unaffected by oCRH or restraint. In contrast, plasma cortisol was unchanged after dehydration, but increased after oCRH and restraint. Moreover, these cortisol responses were significantly greater when the sheep were dehydrated. In Experiment 2, euhydrated sheep (N =6) were infused iv with saline vehicle or vehicle + AVP for a 5-h pretreatment period, followed by a 2-h experimental period in which the animals were injected with 15 \g=m\g oCRH or subjected to 120 min restraint, as in Experiment 1. Blood samples were taken throughout the experiment from a contralateral catheter and the plasma analysed for AVP and cortisol content. The AVP infusion produced plasma levels of the hormone approximately twice those seen after 48 h dehydration in Experiment 1, but did not affect cortisol secretion. Furthermore, the cortisol response to oCRH, or restraint, was not enhanced by the AVP infusion. These results suggest that pituitary responsiveness to exogenous or endogenous CRH (restraint stress) may be enhanced in sheep by dehydration through a mechanism that does not involve an adrenal or pituitary action of circulating AVP.In vitro studies have shown that both CRH and AVP are able to stimulate the secretion of ACTH in preparations of pituitary cells (1,2). Similarly, ex¬ periments using anesthetized rats (3) and conscious sheep (4,5) have demonstrated that concentrations of CRH and AVP in pituitary portal blood increase in response to stress stimuli. The source of these neuropeptide hormones in the rat is the hypophysiotropic CRH neurons originating in the parvocellular part of the hypothalamic paraventricular nucleus (6) and similar neurosecretory pathways are probably also involved in the sheep (7)(8)(9).In addition to these endogenous systems control¬ ling ACTH release, it is well established that exo¬ genous CRH and AVP will stimulate the pituitary/ adrenocortical axis directly in man and synergistic effects of these hormones on ACTH release have also been demonstrated in sheep (10-13). Also, however, studies have been carried out in man where CRH has been given to individuals in whom the release of AVP has been experimentally stimu¬ lated. These investigations have shown that in¬ creasing neurohypophysial AVP secretion by hypertonic saline infusion (14-16), or dehydration (17), enhances the pituitary-adrenocortical re¬ sponse to CRH. Thus, the pituitary effects of exo¬ genous CRH seem to be facilitated under condi¬ tions where the neurosecretory activity of magnocel...

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