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

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.