1. Previous electrophysiological studies have suggested the presence of K Ca and K v channels in human platelets. However, the pharmacology of these channels has not been defined. 2. We have studied potassium channels in human platelets by measuring the efflux of 86 Rb + (a marker for K + ) from 86 Rb + -loaded cells, and have defined their responses to stimulation by the platelet agonist thrombin and the calcium ionophore ionomycin. 3. Thrombin (0.1–0.6 i.u./ml) stimulated an increase in 86 Rb + efflux from the platelets in a concentration-dependent manner. This efflux was significantly inhibited by apamin (100 nmol/l), charybdotoxin (300 nmol/l) and α-dendrotoxin (100–200 nmol/l), blockers of SK Ca channels, K Ch channels and K v channels respectively. Iberiotoxin (300 nmol/l), a specific inhibitor of BK Ca channels, had no effect on the thrombin-stimulated 86 Rb + efflux. Although glibenclamide, an inhibitor of K ATP channels, inhibited the thrombin-stimulated efflux, it did so only in a high concentration (20 μmol/l). 4. Ionomycin (1–5 μmol/l) stimulated an increase in 86 Rb + efflux from the platelets in a concentration-dependent manner. This efflux was significantly inhibited by apamin (100 nmol/l) and charybdotoxin (300 nmol/l). However, iberiotoxin (300 nmol/l) had no effect on the ionomycin-stimulated 86 Rb + efflux. 5. These findings suggest that 86 Rb + efflux from platelets stimulated by thrombin and ionomycin occurs via two types of K Ca channel: SK Ca and K Ch channels. Thrombin also stimulated efflux via K v channels.

1. Na + /K + /2Cl − co-transport mediates a bidirectional symport of Na + , K + and Cl − . The important properties of the co-transport system are its requirement for Na + , K + and Cl − and its inhibition by loop diuretics such as bumetanide. This co-transporter has been described in a number of animal and human tissues. However, its presence in human platelets, although inferred, has not been demonstrated directly. 2. We have studied the efflux of 86 Rb + (a marker for K + ) from Rb + -loaded platelets, and have defined their response to stimulation by high concentrations of external K + . 3. KCl (30–120 mmol/l) stimulated a concentration-dependent increase in 86 Rb + efflux from the platelets. This efflux was completely inhibited by bumetanide (10 μmol/l) but was insensitive to ouabain and R(+)-[(dihydroindenyl)oxy]alkanoic acid. It also required Cl − in the external medium, but did not depend on the presence of extracellular Na + . 4. These observations suggest that 86 Rb + efflux from platelets stimulated by external K + occurs via Na + /K + /2Cl − co-transport acting in a K + /K + (K + /Rb + ) exchange mode. 5. Non-stimulated efflux of 86 Rb + from the platelets (i.e. in the presence of 5 mmol/l K + ) had the characteristics of Na + /K + /2Cl − co-transport acting in normal mode.