Interrelationships between Ca2+ and adenylate and guanylate cyclases in the control of platelet secretion and aggregation.
Interrelationships between Ca2+ and adenylate and guanylate cyclases in the control of platelet secretion and aggregation.
复制标题
Ca2 与腺苷酸和鸟苷酸环化酶在控制血小板分泌和聚集中的相互关系。
DOI：
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发表时间：
1976
影响因子：
11.1
通讯作者：
M. Feinstein
中科院分区：
文献类型：
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作者：
G. Rodan;M. Feinstein
Ca2+ 是基础和前列腺素 E1 (PGE1) 刺激的腺苷酸环化酶 [ATP 焦磷酸裂解酶（环化）] 的强大抑制剂（Ki 等于 16 muM）； EC 4.6.1.1]从匀浆人血小板获得的膜的活性。 Ca2+（但不是离子载体 A23,187）降低了反应的 V(max)，但对 ATP 的 Ks 没有影响。 ATP 和 PGE1 都不影响 Ca2+ 的 Ki。在完整血小板 A23,187 中诱导 Ca2+ 内流，并显着抑制 PGE1 刺激的 3':5'-环单磷酸腺苷 (cAMP) 水平升高。鸟苷酸环化酶[GTP焦磷酸裂解酶（环化）； EC 4.6.1.2]活性主要存在于可溶部分（大于90%）。可溶性酶和膜结合酶均受 Mn2+ 和 Ca2+ 刺激，并受 Zn2+ 抑制。腺苷酸和鸟苷酸环化酶活性均存在于膜级分中。环化酶活性均存在于含有Ca 2+ 激活的ATP酶活性的膜级分中，并且在存在ATP和草酸盐的情况下从培养基中积累Ca 2+ 。其他证据表明这些膜很大程度上起源于血小板的致密管状系统。有人提出，同时抑制腺苷酸环化酶和刺激鸟苷酸环化酶有利于Ca2+对血小板分泌和聚集的直接启动作用。
Ca2+ is a powerful inhibitor (Ki is congruent to 16 muM) of basal and prostaglandin E1 (PGE1)-stimulated adenylate cyclase [ATP pyrophosphate-lyase (cyclizing); EC 4.6.1.1] activity in membranes obtained from homogenized human platelets. Ca2+ (but not the ionophore A23,187) decreased V(max) of the reaction without an effect on the Ks for ATP. Neither ATP nor PGE1 affected Ki for Ca2+. In intact platelets A23,187 induced Ca2+ influx and markedly inhibited PGE1-stimulated rise in adenosine 3':5'-cyclic monophosphate (cAMP) levels. Guanylate cyclase [GTP pyrophosphate-lyase (cyclizing); EC 4.6.1.2] activity was mainly found in the soluble fraction (greater than 90%). Both soluble and membrane bound enzymes were stimulated by Mn2+ and Ca2+ and inhibited by Zn2+. Adenylate and guanylate cyclase activity were both present in a membrane fraction cyclase activity were both present in a membrane fraction which contained Ca2+ activated ATPase activity, and accumulated Ca2+ from the medium in the presence of ATP and oxalate. Other evidence indicates that these membranes originated in large part from the dense tubular system of the platelets. It is proposed that concurrent inhibition of adenylate cyclase and stimulation of guanylate cyclase facilitates the direct initiating effect of Ca2+ on platelet secretion and aggregation.