We studied the effects of dietary sodium on the magnitude of hypertension in sinoaortic denervated (SAD) rats. Groups of SAD rats and sham operated (SO) controls drank tap water and received chows with different amounts of sodium: low (0.08%), regular (0.4%), high (3%) or very high (7%) sodium; other groups, some after unilateral nephrectomy, received regular chow and 1% saline to drink. These various sodium regimens were started before operations and were continued for at least 12 weeks after SAD and SO. Weekly systolic tail-cuff pressures of SAD rats were significantly higher throughout the 12 week postoperative period than those of SO rats regardless of sodium regimen (p less than 0.05 to less than 0.01). Analysis of variance indicated no significant differences between pressures of SAD rats on regular or low sodium chows and those receiving any of the high sodium regimens. When SAD rats were switched from regular to high sodium diets no significant change was induced in systolic pressures. We then examined renal sodium excretion in response to oral sodium loading or to intravenous saline infusion in groups of SAD and SO rats. Both types of studies revealed that SAD rats excreted the extra sodium significantly faster than SO rats. We conclude that hypertension induced by SAD is not dependent on the amount of sodium in the diet and that the magnitude of hypertension is not increased by chronic high sodium intake. The rapid excretion of sodium suggests SAD rats have an enhanced sensitivity to activation and/or to effects of neural and/or humoral factors affecting renal sodium excretion.