Zavoico G B, Cragoe E J
Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115.
J Biol Chem. 1988 Jul 15;263(20):9635-9.
Intracellular free Ca2+ [( Ca2+]i) and pH (pHi) were measured simultaneously by dual wavelength excitation in thrombin-stimulated human platelets double-labeled with the fluorescent probes fura2 and 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein to determine the relationship between changes in [Ca2+]i and pHi, respectively. At 37 degrees C, thrombin (0.5 or 0.1 units/ml) increased [Ca2+]i with no detectable lag period to maximum levels within 13 s followed by a slow return to resting levels. There was a transient decrease in pHi within 9 s that was immediately followed by an alkalinization response, attributable to activation of Na+/H+ exchange, that raised pHi above resting levels within 22 s. At 10-15 degrees C, thrombin-induced changes in [Ca2+]i and pHi were delayed and therefore better resolved, although no differences in the magnitude of changes in [Ca2+]i and pHi were observed. However, the increase in [Ca2+]i had peaked or was declining before the alkalinization response was detected, suggesting that Ca2+ mobilization occurs before activation of Na+/H+ exchange. In platelets preincubated with 5-(N-ethyl-N-isopropyl)amiloride or gel-filtered in Na+-free buffer (Na+ replaced with N-methyl-D-glutamine) to inhibit Na+/H+ exchange, thrombin stimulation caused a rapid, sustained decrease in pHi. Under these conditions there was complete inhibition of the alkalinization response, whereas Ca2+ mobilization was only partially inhibited. Nigericin (a K+/H+ ionophore) caused a rapid acidification of more than 0.3 pH unit that was sustained in the presence of 5-(N-ethyl-N-isopropyl)amiloride. Subsequent stimulation with thrombin resulted in slight inhibition of Ca2+ mobilization. These data show that, in human platelets stimulated with high or low concentrations of thrombin, Ca2+ mobilization can occur without a functional Na+/H+ exchanger and in an acidified cytoplasm. We conclude that Ca2+ mobilization does not require activation of Na+/H+ exchange or preliminary cytoplasmic alkalinization.
用荧光探针fura2和2',7'-双(羧乙基)-5,6-羧基荧光素对人血小板进行双重标记,通过双波长激发同时测量凝血酶刺激的人血小板中的细胞内游离Ca2+([Ca2+]i)和pH(pHi),以分别确定[Ca2+]i和pHi变化之间的关系。在37℃时,凝血酶(0.5或0.1单位/毫升)使[Ca2+]i升高,在13秒内无明显延迟期达到最高水平,随后缓慢恢复到静息水平。在9秒内pHi出现短暂下降,随后立即出现碱化反应,这归因于Na+/H+交换的激活,使pHi在22秒内升高到静息水平以上。在10 - 15℃时,凝血酶诱导的[Ca2+]i和pHi变化延迟,因此更易于分辨,尽管未观察到[Ca2+]i和pHi变化幅度的差异。然而,在检测到碱化反应之前,[Ca2+]i的升高已达到峰值或正在下降,这表明Ca2+动员发生在Na+/H+交换激活之前。在用5-(N-乙基-N-异丙基)amiloride预孵育或在无Na+缓冲液(Na+被N-甲基-D-谷氨酰胺取代)中进行凝胶过滤以抑制Na+/H+交换的血小板中,凝血酶刺激导致pHi迅速、持续下降。在这些条件下,碱化反应完全被抑制,而Ca2+动员仅被部分抑制。尼日利亚菌素(一种K+/H+离子载体)导致快速酸化超过0.3个pH单位,在存在5-(N-乙基-N-异丙基)amiloride的情况下持续存在。随后用凝血酶刺激导致Ca2+动员略有抑制。这些数据表明,在高或低浓度凝血酶刺激的人血小板中,Ca2+动员可以在没有功能性Na+/H+交换体且细胞质酸化的情况下发生。我们得出结论,Ca2+动员不需要Na+/H+交换的激活或细胞质的初步碱化。