1. The effect of intracellular [Ca2+] ([Ca2+]i) on human platelet ion channels was studied using the nystatin whole-cell patch clamp recording technique. 2. Ionomycin-induced increases in [Ca2+]i rapidly activated a voltage-independent K(+)-selective channel with a slope conductance of 30 pS in 154 mM K+ saline. The single-channel conductance decreased in proportion to the square root of the external K+ concentration such that the estimated conductance in 5 mM K+ was approximately 5 pS. 3. The peak current under conditions expected to increase [Ca2+]i to micromolar levels indicated that each platelet possesses a small number (5-7) of 30 pS Ca(2+)-dependent K+ channels (KCa channels). 4. Spontaneous [Ca2+]i spiking was observed in many patch-clamped platelets using fura-2 fluorescence measurements. Each Ca2+ spike triggered up to five KCa channels at any one time. KCa channels were not active at resting levels of [Ca2+]i. 5. The results suggest that platelet KCa channels are not active under resting conditions but may have an important role in determining the membrane potential during Ca2+ signalling.
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机译：1.使用制霉菌素全细胞膜片钳记录技术研究了细胞内[Ca2 +]（[Ca2 +] i）对人血小板离子通道的影响。 2.碘霉素诱导的[Ca2 +] i的增加迅速激活了电压独立的K（+）-选择性通道，在154 mM K +盐水中的斜率电导为30 pS。单通道电导与外部K +浓度的平方根成比例地降低，因此在5 mM K +中的估计电导约为5 pS。 3.在预期将[Ca2 +] i增加到微摩尔水平的条件下的峰值电流表明，每个血小板都具有少量（5-7）的30 pS Ca（2+）依赖性K +通道（KCa通道）。 4.使用fura-2荧光测量，在许多膜片钳紧的血小板中观察到了自发的[Ca2 +] i突增。每个Ca2 +尖峰可随时触发多达五个KCa通道。在[Ca2 +] i的静止水平下，KCa通道不活跃。 5.结果表明，血小板KCa通道在静止条件下不活跃，但可能在确定Ca2 +信号传导期间的膜电位中起重要作用。
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