The Adrenergic System and the Release and Pressor Action of Vasopressin IRENE GAVRAS, SIMON HATINOGLOU, AND HARALAMBOS GAVRAS

We studied the effect of various adrenergic components on vasopressin in groups of anephric rats. Pharmacological interventions included a,-, a2-, and /3-adrenergic receptor blockade and infusions of sodium nitroprusside to achieve a baseline blood pressure fall similar to that obtained by a,-blockade, followed by hypertonic saline infusion to stimulate vasopressin release and administration of a specific V, vascular vasopressin inhibitor to test the degree of blood pressure dependency on vasopressin. The combined hypotensive and osmolar stimuli of nitroprusside followed by hypertonic saline led to the highest level of plasma vasopressin (104 ± 17 pg/ml, p < 0.01) but only a 7 ± 1 mm Hg fall in blood pressure in response to the vasopressin inhibitor. Rats subjected to a,-blockade and saline infusion had the largest blood pressure reduction in response to the vasopressin inhibitor (43 ± 5 mm Hg, p < 0.001), despite a modest rise in vasopressin levels (18 ± 2 pg/ml). Other pharmacological maneuvers produced intermediate responses in terms of vasopressin release and blood pressure response to the vasopressin inhibitor. There was no correlation between vasopressin levels achieved by each maneuver and the magnitude of blood pressure reduction in response to the vasopressin inhibitor. We conclude that 1) plasma levels of vasopressin under these conditions do not permit an accurate estimate of the magnitude of its pressor contribution to the maintenance of a given blood pressure level, which can be demonstrated only by the depressor response to a vasopressin inhibitor, and 2) the maximal vasopressor potential of vasopressin can be expressed only under conditions of impaired a,-adrenergic function. (Hypertension 8 [Suppl II]: 11-163—11-167, 1986)