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% (IC50 = 1.2 nM). This inhibition required the presence of 10 microM 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 (pA2 = 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 (pA2 = 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.
D000067956:Adenylyl Cyclase Inhibitors; D001127:Arginine Vasopressin / Q000494:pharmacology*; D001792:Blood Platelets / Q000201:enzymology*; D006160:Guanosine Triphosphate / Q000494:pharmacology; D006801:Humans; D010974:Platelet Aggregation / Q000187:drug effects; D011956:Receptors, Cell Surface / Q000378:metabolism*; D017483:Receptors, Vasopressin
D000067956:Adenylyl Cyclase Inhibitors; D011956:Receptors, Cell Surface; D017483:Receptors, Vasopressin; D001127:Arginine Vasopressin; D006160:Guanosine Triphosphate