Inulin and mannitol clearances, BUN concentrations and renal morphologic alterations were studied in rats 24 h after the injection of low doses of mercuric chloride. Water drinking rats given 4.7 mg/kg body weight of HgCl2 developed renal failure and severe tubular necrosis. Their clearance of inulin was decreased to the same degree as their simultaneously determined mannitol clearance. Any significant change in tubular permeability should have resulted in a greater loss of mannitol than inulin, and it is suggested that tubular permeability to neither molecule was greatly increased. This is supported by the fact that rats drinking one percent saline in place of tap water for a month prior to receiving the same dose of HgCl2 showed insignificant changes in inulin clearance and minimal elevations in BUN concentration. Nevertheless, histologic sections of their kidneys showed frank tubular necrosis that was equally severe as, but slightly less extensive than that observed in the water drinking rats whose inulin clearance was 6 % of normal. In view of these findings, it seems unlikely that alterationin tubular permeability per se are responsible for the development of acute renal failure in low dose mercury poisoning. The protective effect of salt loading does not depend on the prevention of tubular injury, and may well reflect inhibition of pre-glomerular vasoconstriction by suppression of the renin-angiotensin axis.