Filep J, Rosenkranz B
Thromb Res. 1987 Jan 1;45(1):7-15. doi: 10.1016/0049-3848(87)90252-0.
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.
在富含人血小板的血浆中研究了精氨酸加压素（AVP）诱导聚集的机制。在1.8 - 113.6 mU/ml的范围内，AVP引起剂量依赖性聚集，同时刺激血栓素B2（TXB2）的形成。d(CH2)5Tyr (Me)AVP本身不影响血小板聚集或TXB2释放，但完全抑制AVP的作用。浓度高达280 pM/ml的去氨加压素（DDAVP）对聚集无影响。用维拉帕米、三氟拉嗪或血栓素合成酶阻滞剂甲基咪唑预处理血小板可防止AVP诱导的聚集和TXB2释放。较低浓度的非那吡啶和去甲二氢愈创木酸均不抑制AVP诱导聚集和TXB2释放的能力。这些结果与人类血小板具有钙依赖性血管加压素（V1）亚型的AVP受体这一假设一致，并表明AVP诱导的血小板聚集是通过血栓素释放介导的。
