An analysis of the influence of membrane potential and metabolic poisoning with azide on the sodium pump in skeletal muscle.

Abstract

Activation of the Na pump in muscle [from Rana pipens] by the external K concentration, [K]o, is independent of the membrane potential (Em) as shown by experiments in which Em was either stabilized during variation of [K]o or varied by application of azide at constant or zero [K]o. Application of azide to Na-enriched muscles caused a transient increase in 22Na efflux which occurred either in the presence or in the absence of external K. The increased 22Na efflux induced by azide was abolished by addition of ouabain and was greatly reduced by removal of almost all of the external Na concentration, [Na]o. Azide-treated muscles showed a normal K sensitivity of 22Na efflux and [K]o induced a net Na extrusion from Na-enriched muscles in the presence of azide. Azide reduced ouabain-sensitive K influx to low values thus interfering with the K pump but not with the ability of K to activate the Na pump. Azide promoted a ouabain-sensitive Na-Na exchange in Na-enriched muscles and it partially uncoupled the Na-K exchange normally observed.