Siffert W, Scheid P
Biochem Biophys Res Commun. 1986 Nov 26;141(1):13-9. doi: 10.1016/s0006-291x(86)80327-8.
This study aimed at investigating the mechanisms by which stimulation of human platelets results in activation of Na+/H+ exchange. Platelets were suspended in a slightly buffered medium and the stimulus-induced, amiloride-sensitive H+ release, reflecting Na+/H+ exchange, was estimated from changes in the medium pH. H+ release could be evoked by thrombin and by activators of protein kinase C such as 1-oleoyl-2-acetylglycerol (OAG) or 12-O-tetradecanoylphorbol-13-acetate (TPA). Both the thrombin-and the OAG-induced Na+/H+ exchange could be blocked by trifluoperazine, a protein kinase C inhibitor. The thrombin-induced H+ release was also sensitive to increased intracellular cAMP levels, probably due to inhibition of phospholipase C activation, whereas the OAG-induced activation of Na+/H+ exchange was unaffected. Our data suggest that activation of Na+/H+ exchange is mediated by protein kinase C.
本研究旨在探究刺激人血小板导致钠氢交换激活的机制。将血小板悬浮于轻度缓冲的培养基中，根据培养基pH值的变化估算反映钠氢交换的刺激诱导的、氨氯地平敏感的氢离子释放。凝血酶以及蛋白激酶C激活剂如1-油酰-2-乙酰甘油（OAG）或12-O-十四烷酰佛波醇-13-乙酸酯（TPA）可诱发氢离子释放。凝血酶和OAG诱导的钠氢交换均可被蛋白激酶C抑制剂三氟拉嗪阻断。凝血酶诱导的氢离子释放对细胞内cAMP水平升高也敏感，这可能是由于磷脂酶C激活受到抑制，而OAG诱导的钠氢交换激活则不受影响。我们的数据表明，钠氢交换的激活是由蛋白激酶C介导的。
