Mechanism of vasopressin-induced platelet aggregation

The mechanism of aggregation induced by arginine vasopressin (AVP) was studied in human platelet rich plasma. AVP--over the range of 1.8-113.6 mU/ml--caused a dose-dependent aggregation with a concomitant stimulation of thromboxane B2 (TXB2) formation. d(CH2)5Tyr (Me)AVP did not by itself affect platelet aggregation or TXB2 release, but completely inhibited the action of AVP. DDAVP up to the concentration of 280 pM/ml had no effect on aggregation. Pretreatment of platelets with verapamil, trifluoroperazine or methylimidazole, a thromboxane synthetase blocker, prevented AVP-induced aggregation and TXB2 release. Neither phenidone in lower concentration nor nordihydroguaiaretic acid inhibited the ability of AVP to induce aggregation and TXB2 release. These results are consistent with the hypothesis that human platelets possess AVP receptor of the calcium-dependent vasopressor (V1) subtype and suggest that AVP-induced platelet aggregation is mediated via thromboxane release.