Key result
Ca2+-activated K+ channels exist in human platelets, are apamin insensitive and charybdotoxin sensitive, and may contribute to the resting membrane potential.
This study demonstrates the presence of charybdotoxin-sensitive, apamin-insensitive calcium-activated potassium channels in human platelets that contribute to resting membrane potential.
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Hypothesis-generating for platelet K+ channels; leaves open any role in human thrombosis or therapy.
The cationic fluorescent probe, DiSC3(5) was used to measure the membrane potential in human platelets. Hyperpolarization was induced by the addition of Ca2+ to the medium and also by the addition of the Ca2+ ionophore, A23187. In the absence of extracellular Ca2+ ([Ca2+]o) there was no response to A23187. The threshold concentration for [Ca2+]o was 20 microM and for A23187 was 12 nM. The increase polarity induced by [Ca2+]o was not affected by various K+ channel blockers. However, the effect of A23187 was inhibited by quinine and charybdotoxin, while apamin, tetraethylammonium, and the calmodulin inhibitors trifluoperazine and compound R24571 were ineffective. The resting membrane potential was -66 +/- 0.9 mV and was decreased by quinine. There are three conclusions from this study: (i) Ca2+-activated K+ channels exist in human platelets; (ii) they are the type that are apamin insensitive, charybdotoxin sensitive; and (iii) they may contribute to the resting membrane potential.
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Fine et al. (1989) studied this question. Ca2+ and Ca2+ ionophore A23187 vs. Absence of extracellular Ca2+ was evaluated on Membrane potential and hyperpolarization. Ca2+-activated K+ channels exist in human platelets, are apamin insensitive and charybdotoxin sensitive, and may contribute to the resting membrane potential.
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