Sage S O, Merritt J E, Hallam T J, Rink T J
Physiological Laboratory, University of Cambridge, U.K.
Biochem J. 1989 Mar 15;258(3):923-6. doi: 10.1042/bj2580923.
Previous studies of the early kinetics of rises in cytosolic free [Ca2+] in fura-2-loaded human platelets suggested that: (1) Ca2+ entry slightly preceded internal discharge with thrombin and other agonists known to promote inositol lipid hydrolysis; (2) with ADP, Ca2+ entry occurred without measurable delay and clearly preceded internal Ca2+ discharge. In the present work, Mn2+ added to the external medium was used as a marker for Ca2+ entry. By using an excitation wavelength of 360 nm, a quench of fura-2 can be followed to report Mn2+ entry without 'contamination' of the signal by changes in [Ca2+], because at this isosbestic wavelength Ca2+ does not alter fura-2 fluorescence. The present results show that, with thrombin stimulation, readily discernible Mn2+ entry starts after discharge of internal Ca2+ and is maintained for many minutes. With ADP, Mn2+ entry starts without measurable delay (less than 20 ms) and clearly precedes internal Ca2+ discharge. However, the enhanced Mn2+ permeability is only short-lived. These results, considered alongside previous data, point to the possible presence of at least three different receptor-mediated Ca2+-entry mechanisms in human platelets, one of which may include regulation by the 'state of filling' of this dischargeable Ca2+ store.
先前对用fura - 2负载的人血小板中胞质游离[Ca2+]升高的早期动力学研究表明:(1) Ca2+内流略先于用凝血酶和其他已知能促进肌醇脂质水解的激动剂引起的内部释放;(2) 对于ADP,Ca2+内流无明显延迟地发生,且明显先于内部Ca2+释放。在本研究中,添加到外部介质中的Mn2+用作Ca2+内流的标志物。通过使用360 nm的激发波长,可以跟踪fura - 2的淬灭以报告Mn2+内流,而不会因[Ca2+]的变化而“污染”信号,因为在这个等吸收波长下Ca2+不会改变fura - 2的荧光。目前的结果表明,在凝血酶刺激下,在内部Ca2+释放后开始出现明显的Mn2+内流,并持续许多分钟。对于ADP,Mn2+内流无明显延迟地开始(小于20毫秒),且明显先于内部Ca2+释放。然而,增强的Mn2+通透性只是短暂的。这些结果与先前的数据一起考虑,表明人血小板中可能存在至少三种不同的受体介导的Ca2+内流机制,其中一种可能包括受这种可释放Ca2+储存库的“充盈状态”调节。