Siffert W, Mückenhoff K, Scheid P
Biochem Biophys Res Commun. 1984 Dec 28;125(3):1123-8. doi: 10.1016/0006-291x(84)91400-1.
We have investigated the release of protons from human platelets and platelet aggregation induced by the calcium ionophore, A 23187. Addition of the ionophore to suspensions of washed platelets resulted in fast liberation of H+. In the presence of 0.2 mM amiloride, a potent inhibitor of Na+/H+ countertransport, the amount of protons liberated was decreased by 50% and was further reduced to about 10% by 1 mM amiloride. Similar inhibition of H+-release was observed after decreasing Na+ in the incubation medium. Both results suggest that increasing internal Ca2+ by the ionophore induces Na+/H+ exchange in human platelets. Platelet aggregation could be induced by adding the ionophore to the platelet suspension. This aggregation was inhibited by amiloride, at least when induced by low ionophore concentrations. The results suggest that stimulation of Na+/H+ exchange, and the concomitant increase in intraplatelet pH, are important mechanisms in platelet activation.
我们研究了人血小板中质子的释放以及钙离子载体A 23187诱导的血小板聚集。将该离子载体添加到洗涤过的血小板悬液中会导致H⁺快速释放。在存在0.2 mM氨氯吡咪（一种有效的Na⁺/H⁺逆向转运抑制剂）的情况下，释放的质子数减少了50%，而1 mM氨氯吡咪则使其进一步减少至约10%。在孵育培养基中降低Na⁺后，也观察到了对H⁺释放的类似抑制作用。这两个结果都表明，离子载体增加细胞内Ca²⁺会诱导人血小板中的Na⁺/H⁺交换。向血小板悬液中添加离子载体可诱导血小板聚集。这种聚集受到氨氯吡咪的抑制，至少在低离子载体浓度诱导时是如此。结果表明，刺激Na⁺/H⁺交换以及伴随的血小板内pH值升高是血小板激活的重要机制。
