Vasopressin inhibits the adenylate cyclase activity of human platelet particulate fraction through V1‐receptors

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Abstract
Arg8-vasopressin inhibited the adenylate cyclase activity of human platelet particulate fraction up to a maximum of 27% (IC 50 = 1.2 nM). This inhibition required the presence of 10 μM GTP and was optimal with 100 mM NaCl. Orn8-vasopressin had similar effects. 1-Deamino-Val4, D-Arg8-vasopressin did not by itself affect adenylate cyclase activity but competitively inhibited the action of Arg8-vasopressin (pA 2 = 7.74). Arg8-vasopressin did not inhibit adenylate cyclase in intact platelets but instead caused platelet aggregation, an effect that was also competitively inhibited by 1-deamino-Val4, D-Arg8-vasopressin (pA 2 = 7.82). Thus, platelets possess vasopressin receptors of the V1 type that, under appropriate conditions, can mediate either inhibition of platelet adenylate cyclase or platelet aggregation.