In human subjects cortisol raises the osmotic threshold for vasopressin release. The presumption that this results from a direct inhibitory action of cortisol on osmotically stimulated vasopressin release has been tested in conscious rhesus monkeys. Preparatory surgical procedures included chronic bladder catheterization, placement of cannulae in the right atrium, the left jugular vein and the stomach and stereotaxic insertion of metal cannulae in both supraoptic nuclei. The osmotic threshold for vasopressin release was defined as the plasma osmolality at the beginning of the 3 min urine sample in which free water clearance first fell by >2 SD below the mean control level, in response to 5% saline infusion during constant hydration. Compared with control substances (0.9% saline solution or 11-deoxycortisol crystals), cortisol solution or crystals introduced into both supraoptic nuclei significantly lowered the plasma osmolality during the water-induced pre-saline diuresis, so that a larger amount of 5% NaCl infusion was required to reach the osmotic threshold. Thus, cortisol introduced into the supraoptic nuclei prolonged the duration of 5% saline infusion needed to reach the osmotic threshold, and raised the increment in plasma osmolality needed to reach the threshold but cortisol did not significantly raise the absolute level of the threshold.
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