The relationship between the concurrent increase in net K+ efflux and isometric tension development has been studied in perifused dog saphenous vein strips using 86Rb+ as a marker for K+. Noradrenaline, acting through alpha-adrenoceptors, or depolarization induced by raised extracellular K+ (in the presence of an alpha-adrenoceptor antagonist) increased both 86Rb+ efflux and isometric tension. However, even with a high concentration of K+ (120 mmol l-1) the evoked changes in 86Rb+ efflux and tension were small compared with those produced by noradrenaline. There was a linear relationship between 86Rb+ efflux and tension maintained throughout the time course of each evoked response. This linear relationship was the same for each response evoked throughout the concentration range of noradrenaline (1-100 mumol l-1) or K+ (30-120 mmol l-1) used. Substitution of extracellular Ca2+ by Ba2+ did not alter either basal tension or 86Rb+ efflux; nor did it alter either the magnitude of noradrenaline-evoked changes in 86Rb+ efflux or tension, or the slope of the relationship between the two seen with Ca2+. The cardioactive steroid, acetylstrophanthidin, altered the evoked response to exogenous noradrenaline and to K+ depolarization in that there was now a significant increase in 86Rb+ efflux relative to tension, although the linear relationship between the two was maintained. In the nominal absence of extracellular Ca2+ the increase in 86Rb+ efflux produced by exogenous noradrenaline was maintained but the evoked increased in tension was reduced. The data shows for dog saphenous vein: (a) that gross evoked 86Rb+ efflux is attenuated by an active backflux mediated by the sodium-potassium pump and (b) that 86Rb+ efflux can occur through a membrane potential-activated pathway and through an independent alpha-adrenoceptor-activated pathway but although the linear relationship between 86Rb+ efflux and tension can be best explained by their co-dependence upon Ca2+, the present experiments provide no objective evidence for an internal calcium-activated pathway.