1. Human platelets were studied using a combination of patch‐clamp and fluorescent indicators of membrane potential and [Ca2+]i. 2. Whole‐cell and cell‐attached patch recordings showed voltage‐gated channels selective for K+ (IK(V]. These channels were activated by depolarization at a threshold close to the platelet resting potential and were blocked by the venom charybdotoxin (CTX; 10‐20 nM). Several different conductance states were observed, ranging from 5 to 34 pS, with isotonic KCl in the patch pipette and bath. 3. Measurements with the potential‐sensitive dye 3,3'‐dipropylthia‐dicarbocyanine, diS‐C3‐(5), in platelet suspensions showed that CTX depolarized the resting potential by approximately 25 mV. Thus, CTX‐sensitive, voltage‐gated K+ channels appear to play a major part in setting the resting potential. 4. ADP‐evoked Ca2+ influx, monitored with Fura‐2, was reduced by 10 nM‐CTX. Restoration of a large negative membrane potential with valinomycin reversed this effect of CTX. These results suggest that the Ca2+ influx depends on the negative membrane potential and that K+ channels may be important in maintaining this potential during activation.

Mahaut‐Smith, M. P., Rink, T. J., Collins, S. C., & Sage, S. O. (1990). Voltage‐gated potassium channels and the control of membrane potential in human platelets. The Journal of Physiology, 428(1), 723–735. Portico.