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In anesthetized dogs, perfusion of the cerebral ventricles with indomethacin (IM), an inhibitor of prostaglandin biosynthesis, at rates of 1.9 or 7.6 microgram/min was without effect on the plasma ADH concentration. Ventriculo-cisternal perfusion with angiotensin II (AII; 19 ng/min) resulted in a 3-fold increase in the plasma ADH concentration within 45 min. When AII and IM were perfused together, the plasma ADH concentration increased only 2-fold, a response which was significantly lower than that obtained with AII alone. Thus, the ability of central AII to stimulate ADH release may depend, at least in part, upon the local release of prostaglandins.
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