The Effect of Intracerebroventricular Indomethacin on Osmotically Stimulated Vasopressin Release

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Abstract
Experiments investigated the effect of intracerebroventricular administration of a prostaglandin synthesis inhibitor on the osmotic control of vasopressin (ADH) secretion. During ventriculocisternal perfusion with indomethacin (7.6 .mu.g/min) or vehicle, dogs were infused i.v. with either 2.5 or 0.15 M NaCl. Hypertonic saline infusion elevated plasma osmolality .apprx. 60 mosm/kg H2O. In accordance, the plasma ADH concentration increased substantially in animals perfused ventriculocisternally with the vehicle (from 2.1 .+-. 0.7 to 7.3 .+-. 1.3 .mu.U/ml); this response was markedly attenuated in animals perfused with indomethacin (from 1.0 .+-. 0.2 to 2.2 .+-. 0.4 .mu.U/ml). Isotonic saline infusion caused a decline in plasma ADH concentration which was similar in the indomethacin- and vehicle-perfused groups. Mean arterial blood pressure was unchanged during the experiments. In a companion study, ventriculocisternal perfusion with 152 ng prostaglandin E2/min was as effective in stimulating ADH release in the presence of indomethacin as in its absence, indicating that the action of indomethacin in the 1st study was not nonspecific. The suppression of osmotically induced ADH release by intracerebroventricular indomethacin suggests that endogenous brain prostaglandins play a critical intermediary role in the osmotic control of ADH secretion.