Coupling between platelet 5-hydroxytryptamine and potassium transport.

Platelet plasma membrane vesicles accumulate 5-hydroxytryptamine in response to a gradient of NaCl (out > in). Although potassium ion is not required for this process, a K’ concentration gradient (in > out) elevates the steady state level of 5-hydroxytryptamine accumulation 5-fold. Transport is independent of the generation of an electrical potential (interior negative) across the vesicle membrane when K’ is present internally, but in its absence 5-hydroxytryptamine transport is apparently electrogenic, with net positive charge crossing the membrane with 5-hydroxytryptamine. Potassium ion directly interacts with the 5-hydroxytryptamine transporter as evidenced by its effects on the initial rate of 5-hydroxytryptamine transport. Internal K+ stimulates influx and external K’ inhibits. Even in the absence of a K’ gradient, K’ affects the kinetics of 5-hydroxytryptamine transport, 30 meq of K’/liter increasing the V,,,,, for 5-hydroxytryptamine transport 3-fold and increasing K,,, by 2fold. The unidirectional efflux of [3H]5-hydroxytryptamine is stimulated by both K’ and unlabeled 5-hydroxytryptamine in the external medium. Although 5hydroxytryptamine-stimulated efflux requires external Na+, K’-induced efflux is independent of external Na’. A mechanism consistent with the above observations is proposed in which internal K+ accelerates the influx of 5-hydroxytryptamine by increasing the rate at which the 5-hydroxytryptamine binding site of the transporter “moves” from the internal surface of the membrane to the external surface. Concomitant with this movement, one potassium ion is transported from the vesicle lumen to the external medium.