Effects of High External Concentrations of K⁺ on ⁸⁶Rb⁺ Efflux in Human Platelets: Evidence for Na⁺/K⁺/2Cl⁻ Co-Transport

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 ⁸⁶Rb⁺ (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 ⁸⁶Rb⁺ 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 ⁸⁶Rb⁺ 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 ⁸⁶Rb⁺ 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.