Nishio H, Ikegami Y, Nakata Y, Segawa T
Department of Pharmacology, Hiroshima University School of Medicine, Japan.
Neurochem Int. 1993 Feb;22(2):205-10. doi: 10.1016/0197-0186(93)90014-v.
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.
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。