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二磷酸腺苷(ADP)诱导人血小板膜电位去极化。

ADP induced depolarization of human platelet membrane potential.

作者信息

Wencel-Drake J D, Feinberg H

出版信息

Thromb Haemost. 1985 Feb 18;53(1):75-9.

PMID:4039475
Abstract

The transmembrane potential of human blood platelets suspended in plasma was investigated by studying the distribution of a radiolabeled permeant ion [14C] thiocyanate. The membrane potential of resting platelets was found to be -54.50 mV +/- 9.23 S.D. with a range of -39 to -76 mV (n = 27). The possibility that platelet activation alters membrane potential or that changes in membrane potential serve as an activation trigger was investigated. Stimulation by ADP (10 microM) resulted in a significant (p less than 0.05) depolarization of the membrane potential. Preincubation with 6 mM EGTA failed to inhibit ADP-induced depolarization even though EGTA effectively prevented primary and secondary aggregation but not shape change. Preincubation with PGE1 inhibited shape change, aggregation, and the ADP-induced depolarization. No significant change in membrane potential was observed following stimulation by epinephrine (50 microM). These results suggest that the initial interaction of ADP and its receptor may involve an inward positive current which can be determined by thiocyanate distribution.

摘要

通过研究放射性标记的通透离子[14C]硫氰酸盐的分布,对悬浮于血浆中的人体血小板的跨膜电位进行了研究。发现静息血小板的膜电位为-54.50 mV±9.23标准差,范围为-39至-76 mV(n = 27)。研究了血小板激活改变膜电位或膜电位变化作为激活触发因素的可能性。ADP(10微摩尔)刺激导致膜电位显著(p小于0.05)去极化。用6毫摩尔乙二醇双乙醚二胺四乙酸(EGTA)预孵育未能抑制ADP诱导的去极化,尽管EGTA有效地阻止了初级和次级聚集,但未阻止形状改变。用前列腺素E1(PGE1)预孵育可抑制形状改变、聚集以及ADP诱导的去极化。肾上腺素(50微摩尔)刺激后未观察到膜电位有显著变化。这些结果表明,ADP与其受体的初始相互作用可能涉及内向正电流,这可以通过硫氰酸盐分布来确定。

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