In an attempt to determine whether prostaglandin E2 (PGE2) can act centrally to affect the release of vasopressin (ADH), the ventriculo-cisternal system of anaesthetized dogs was perfused with PGE2. When PGE2 was perfused at a rate of 76·4 ng/min (0·19 ml/min), the plasma ADH concentration was unchanged. However, perfusion of PGE2 at a rate of 152·8 ng/min (0·19 ml/min) resulted in a significant increase in the plasma ADH concentration from the control value of 9·0 ± 2·2 (s.e.m.) to 18·8 ± 3·9 μu./ml at 10 min and to 41·0 ± 16·7 μu./ml at 30 min after the start of the perfusion. There were no changes in arterial blood pressure, rectal temperature, plasma osmolality, and the plasma concentrations of sodium and potassium. In additional experiments, i.v. injection of indomethacin (2 or 20 mg/kg) decreased the plasma ADH concentration by approximately 50%. Although this finding is consistent with a role of PGE2 in the control of ADH release, it could also have been due to the observed increases in arterial blood pressure and effective left atrial pressure. Plasma renin activity was unchanged in the indomethacin experiments. It is concluded that PGE2 can act in the central nervous system to stimulate ADH release.
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