NI2+ IMPAIRS THROMBIN-INDUCED SIGNAL-TRANSDUCTION BY ACTING ON THE AGONIST AND OR RECEPTOR IN HUMAN PLATELETS

被引：17

作者：

AZULA, FJ

ALONSO, R

MARINO, A

TRUEBA, M

MACARULLA, JM

机构：

来源：

AMERICAN JOURNAL OF PHYSIOLOGY | 1993年 / 265卷 / 06期

关键词：

PHOSPHOLIPASE-C; CALCIUM; CALCIUM IONOPHORES; PROTEIN KINASE-C; PHORBOL ESTER; STAUROSPORINE; PLATELET AGGREGATION;

D O I：

10.1152/ajpcell.1993.265.6.C1681

中图分类号：

Q4 [生理学];

学科分类号：

071003 ;

摘要：

We have investigated the effect of NiCl2 on platelet activation induced by thrombin, phorbol 12-myristate 13-acetate, and calcium ionophores. Besides blocking Ca2+ influx, NiCl2 inhibited platelet aggregation, intracellular Ca2+ mobilization, and phospholipase C activation induced by thrombin in a dose-dependent manner. In contrast to ionomycin, NiCI2 Completely blocked the platelet aggregation and intracellular Ca2+ mobilization induced by A23187. A23187 was not able to translocate Ni2+ across the plasma membrane. Ni2+ also inhibited phorbol myristate acetate-induced platelet aggregation. The results with staurosporine and low NiCl2 concentrations are in agreement in that increases in intracellular Ca2+ concentration and protein kinase C activation are necessary for full platelet activation mediated by thrombin.

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收藏

页码：C1681 / C1688

页数：8

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