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Decreased activity of the electrogenic sodium pump of vascular smooth muscle has been reported in several forms of experimental hypertension and may play an important role in basic disease mechanisms. It has been proposed that such pump suppression may characterize volume-expanded forms of hypertension. The present investigation tested this latter hypothesis. Sodium pump activity was assessed in vitro in sodium-loaded tail artery and thoracic aorta freshly excised from Dahl salt-sensitive (S) and salt-resistant (R) rats on low (0.4%) or high (8%) NaCl diets for 5 to 7 weeks. Rubidium (86Rb) uptake in the absence (total uptake) and presence (ouabain-insensitive uptake) of 1.0mM ouabain was measured and ouabain-sensitive uptake (nmole/mg dry weight/10 min) was calculated. In S rats, salt feeding was accompanied by elevation of arterial pressure, cardiac hypertrophy, increases of 20% to 30% in total blood volume, and increases in the ouabain-sensitive, ouabain-insensitive, and total uptakes in the aorta, but no significant change in uptakes in the tail artery. However, ouabain-sensitive uptake in the tail artery of all S rats exceeded than in R rats. There was no evidence of a decrease in vascular sodium pump activity accompanying hypertension in either artery. Therefore, the results of this study provide no evidence in support of the hypothesis that pump suppression in vascular smooth muscle characterizes volume-expanded forms of hypertension. It is unlikely that the observed increases in vascular pump activity in S rats reflected intracellular sodium concentrations higher than those in the control rats. Rather, increases in the numbers of pump molecules or in their turnover rate are probably involved.