Pulcinelli F M, Daniel J L, Riondino S, Gazzaniga P P, Salganicoff L
Dept. of Experimental Medicine, University La Sapienza, Rome, Italy.
Thromb Haemost. 1995 Feb;73(2):304-8.
In a suspension of thrombin degranulated platelets (TDP), ADP and epinephrine can induce platelet aggregation, whereas the synthetic agonist of the thromboxane/endoperoxide receptor U46619 causes only shape change. However, U46619 can enhance platelet aggregation induced by ADP and epinephrine. In this paper, we have measured fibrinogen binding in relation to phospholipase C (PLC) activation and calcium mobilization in TDP activates by ADP, epinephrine and U46619. ADP caused fibrinogen binding in TDP but neither activated PLC nor caused a calcium mobilization. The requirement for ADP in inducing exposure of fibrinogen binding sites was not absolute since the combination of epinephrine and U46619 produced an increase in fibrinogen binding. U46619 caused significant PLC activation and cytosolic calcium release but not fibrinogen binding. These results suggest that in TDP the exposure of fibrinogen binding sites, after agonist activation, is independent of both PLC activation and calcium mobilization.
在凝血酶脱颗粒血小板（TDP）悬液中，ADP和肾上腺素可诱导血小板聚集，而血栓素/内过氧化物受体的合成激动剂U46619仅引起形态改变。然而，U46619可增强ADP和肾上腺素诱导的血小板聚集。在本文中，我们测定了在由ADP、肾上腺素和U46619激活的TDP中，与磷脂酶C（PLC）激活和钙动员相关的纤维蛋白原结合情况。ADP导致TDP中的纤维蛋白原结合，但既不激活PLC也不引起钙动员。诱导纤维蛋白原结合位点暴露对ADP的需求并非绝对，因为肾上腺素和U46619的组合可使纤维蛋白原结合增加。U46619引起显著的PLC激活和胞质钙释放，但不引起纤维蛋白原结合。这些结果表明在TDP中，激动剂激活后纤维蛋白原结合位点的暴露与PLC激活和钙动员均无关。
