The Na+-K+pump activity was determined in femoral arterial smooth muscle from deoxycorticosterone acetate (DOCA)-salt hypertensive rats using potassium relaxation and ouabainsensitive86Rb uptake as indices. The membrane-stabilizing effect of calcium and its relation to Na+-K+pump activity also were examined. Femoral arteries from DOCA-saJt rats exhibited a greater relaxation in response to potassium addition after contraction with norepinephrine in a low potassium (0.6 mM) Krebs solution. The concentration of potassium required to produce a 50% relaxation was significantly less in DOCA-salt rats. Ouabain-sensitive86Rb uptake was significantly greater at 3,10, and 20 minutes of86Rb incubation in femoral arteries from DOCA-salt rats. Linear regression analysis revealed a significant correlation between the uptake of86Rb and time of incubation in both control and DOCA-salt rats. A significant difference in the slopes of the regression lines showed that the rate of uptake was greater in DOCA-salt rats. No difference was observed in ouabain-insensitive86Rb uptake. A dose-dependent relaxation in response to increasing concentrations of calcium following contraction to norepinephrine was observed in femoral arteries from control and DOCA-salt rats. The relaxation was directly dependent on the level of extracellular potassium and was blocked by ouabain. Femoral arteries from DOCA-salt rats relaxed to a significantly greater extent in response to calcium at each level of potassium when compared with controls. These results provide further evidence for an increase in Na+-K+pump activity in vascular smooth muscle from DOCA-salt hypertensive rats. In contrast to previous reports, however, calcium-induced relaxation was shown to be increased in the DOCA-salt rat. This effect is directly dependent on the activity of the Na+-K+pump and supports observations of increased potassium relaxation and86Rb uptake.