Calcium-Activated Potassium Channels in Human Platelets

Abstract

The cationic fluorescent probe, DiSC,(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+ ([Ca'+],) there was no response to A23187. The threshold concentration for [Ca2+]., was 20 fiM and for A23187 was 12 nM. The increase polarity induced by [Ca2+lO 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 trifluoperarine and compound I324571 were ineffective. The resting membrane potential was -66 f 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. [P.S.E.B.M. 1989[P.S.E.B.M. , VoI 1921 nimal cell plasma membranes possess K+ channels, which, when opened, induce cytoplasmic

Pharmacological Evidence of Calcium-Activated and Voltage-Gated Potassium Channels in Human Platelets

“…2), suggesting the presence of Kch channels (which may be IKca channels) in human platelets. This is in agreement with a number of earlier studies on Kca channels in human platelets [5,6,91, which have demonstrated the presence of charybdotoxin-sensitive K+ channels. Furthermore, apamin (100 nmol/l) and charybdotoxin (300nmol/l) added together had a greater effect on thrombin-stimulated 8GRb+ efflux than either alone (Fig.…”

“…2), suggesting the presence of apamin-sensitive SKc, channels in human platelets. In an earlier study, Fine et al [5] measured changes in platelet membrane potential stimulated by the Ca2+ ionophore A23187 in the presence of various Kca channel inhibitors, but found no evidence for the presence of apamin-sensitive K+ channels in human platelets. However, in their experiments apamin was used in a concentration of 25 nmol/l, and the toxin was incubated with the cells for only 2min.…”

Reversible inhibition of the platelet procoagulant response through manipulation of the Gardos channel

“…A number of studies have demonstrated the presence of both voltage-operated K ϩ channels and Ca 2ϩ -induced K ϩ channels in the plasma membrane of platelets. [27][28][29][30] The latter can be subdivided in 3 different types, SK (small conductance), IK (intermediate conductance) and BK (large conductance) channels. [31][32][33] Whether or not all 3 types are present in platelets is presently unknown.…”

Characterization of Na+‐K+ homeostasis of cultured human skin fibroblasts in the presence and absence of fetal bovine serum

“…The rising intracellular Ca++, in concert with activation of the calmodulin system, produces accelerated K+ efflux and enhanced Na+ influx. Indeed, Ca++ activated K + channels have been described in several cell types (Gardos, 1958;Putney et al, 1978;Kurtzer and Roberts, 1982;Martin and Gordon, 1983;Hoffman et al, 1984;Fine et al, 1989). Although we did not have a direct measure of Cai+ activated K + channels, it is possible that the activation of this transport system is ultimately responsible for the enhanced K+ efflux following FBS removal.…”