Calcium-activated potassium channels in human platelets.

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.