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血清素诱导的细胞内钙离子浓度升高与血小板中钙离子内流刺激之间的关系。

Relationships between serotonin induced elevation of intracellular Ca2+ concentration and stimulation of Ca2+ influx in blood platelets.

作者信息

Nishio H, Ikegami Y, Nakata Y, Segawa T

机构信息

Department of Pharmacology, Hiroshima University School of Medicine, Japan.

出版信息

Neurochem Int. 1993 Feb;22(2):205-10. doi: 10.1016/0197-0186(93)90014-v.

Abstract

Serotonin (5-HT) caused immediate elevation of intracellular Ca2+ concentration ([Ca2+]i) in blood platelets, and it was completely inhibited by 1 mM EGTA. In Ca2+ replenished platelets, however, 2 mM EGTA did not affect the 5-HT induced elevation of [Ca2+]i when EGTA was applied just before or during the stimulation by 5-HT. At the same concentration 5-HT was also found to enhance Ca2+ influx through the activation of 5-HT2 receptor, but with rather longer latent time. From these results it is suggested that 5-HT induced elevation of [Ca2+]i is caused by mobilization of Ca2+ from intracellular Ca2+ storage sites, but not by direct stimulation of Ca2+ influx. Depletion of such Ca2+ stores might impair the effect of 5-HT on [Ca2+]i. Thus, 5-HT induced augmentation of Ca2+ influx might be secondary to replenishment of the depleted Ca2+ stores which was caused by 5-HT induced internal release of Ca2+. It is concluded that the effects of 5-HT on [Ca2+]i and Ca2+ influx in platelets are manifested sequentially or independently.

摘要

血清素(5-羟色胺,5-HT)可使血小板内细胞内钙离子浓度([Ca2+]i)立即升高,且这种升高可被1 mM的乙二醇双四乙酸(EGTA)完全抑制。然而,在补充了钙离子的血小板中,当在5-HT刺激前或刺激过程中加入2 mM EGTA时,其并不影响5-HT诱导的[Ca2+]i升高。同样浓度的5-HT还被发现可通过激活5-HT2受体增强钙离子内流,但潜伏期相对较长。从这些结果表明,5-HT诱导的[Ca2+]i升高是由细胞内钙离子储存位点释放钙离子所致,而非直接刺激钙离子内流。此类钙离子储存的耗竭可能会削弱5-HT对[Ca2+]i的作用。因此,5-HT诱导的钙离子内流增加可能是5-HT诱导的钙离子内源性释放导致的钙离子储存耗竭后补充的结果。得出的结论是,5-HT对血小板中[Ca2+]i和钙离子内流的作用是依次或独立表现的。

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