Increased dietary salt in rats has been shown to sensitize central sympathetic circuits and enhance sympathetic responses to several stressors, including hyperinsulinemia, intracerebroventricular injection of angiotensin and electrical stimulation of sciatic nerve afferents. These findings prompted us to test the hypothesis that increased dietary salt enhanced the exercise pressor reflex.Male Sprague-Dawley rats were fed 0.1% (n=16) or 4.0% (n=18) NaCl chow for 14-21 days. Then, rats were decerebrated and the exercise pressor reflex was produced by static contraction of the hindlimb muscles through electrical stimulation of the cut peripheral ends of the L4 and L5 ventral roots. We found that contraction produced a significantly greater increase in mean arterial pressure of rats fed 4.0% NaCl (24±2 mmHg) versus 0.1% NaCl (15±2 mmHg). Baseline mean arterial pressure was not different between 0.1% versus 4.0% NaCl diets (79±5 vs 83±4 mmHg). The tension time indices were not different between the 0.1% (17±1 kg per s) versus 4.0% (18.2±2 kg s) NaCl groups (P = 0.422). The enhanced responsiveness to contraction appeared to be attributable to sensitized group III mechanoreceptors because the renal and lumbar sympathetic responses to contraction were augmented within 200 ms of the onset of contraction. Section of the L4 and L5 dorsal roots abolished the pressor responses to contraction in both groups of rats, an effect showing that the responses were reflex in origin. We conclude that increased dietary salt can enhance the reflex sympathetic responses to static exercise.