Stimulus-response coupling in human platelets. Changes evoked by platelet-activating factor in cytoplasmic free calcium monitored with the fluorescent calcium indicator quin2.
Stimulus-response coupling in human platelets. Changes evoked by platelet-activating factor in cytoplasmic free calcium monitored with the fluorescent calcium indicator quin2.
复制标题
人血小板中的刺激-反应耦合。
作者：
T. Hallam;A. Sanchez;T. Rink
研究了载钙荧光指示剂quin2的人血小板中胞质游离钙[Ca2+]i的变化在血小板活化因子（PAF）应答中的作用。在1 mM外钙存在的情况下，PAF在几秒钟内使[Ca2+]升高8-10倍，在1微米附近达到峰值。[Ca2+]i随后在几分钟内下降到基础水平。在缺乏外源钙的情况下，[Ca2+]i的增加幅度要小得多。这些发现表明PAF增加[Ca2+]部分是由于内部Ca2+的放电，但主要是受刺激的内流。阿司匹林阻断环加氧酶仅能轻微降低[Ca2+]i的变化，表明血栓素A2不是钙运动的主要介质。在对照条件下，PAF能刺激细胞的形态变化、聚集和分泌。环加氧酶阻断使聚合和分泌量减少一半。在[Ca2+]i上升很小或受到抑制的情况下，形状变化和分泌仍然发生，这表明细胞内激活剂的作用不仅仅是Ca2+。讨论了磷酸肌苷分解产物的可能参与。
The role of changes in cytoplasmic free calcium, [Ca2+]i, in the responses to platelet-activating factor (PAF) was studied in human platelets loaded with the fluorescent calcium indicator, quin2. In the presence of 1 mM external calcium, PAF raised [Ca2+]i 8-10-fold in a few seconds to peak near 1 microM. [Ca2+]i then declined over several minutes towards the basal level. In the absence of external calcium there was a much smaller increase in [Ca2+]i of similar pattern. These findings suggest that PAF increases [Ca2+]i partly by discharge of internal Ca2+, but mainly by stimulated influx. Blockade of cyclo-oxygenase with aspirin only slightly reduced the [Ca2+]i changes, indicating that thromboxane A2 is not a major mediator of the calcium movements. In control conditions PAF could stimulate shape-change, aggregation and secretion. Aggregation and secretion were roughly halved by blockade of cyclo-oxygenase. Shape-change and secretion still occurred under conditions where the [Ca2+]i rise was small or suppressed, indicating a role for intracellular activators other than Ca2+. The possible involvement of products of phosphoinositide breakdown is discussed.