Intravenous infusion of the natriuretic drug furosemide in sheep led to the excretion of large quantitites of hypotonic urine. The sheep consumed more water than was needed simply to restore osmotic equilibrium. The stimulus for the additional intake was presumably hypovolemia resulting from the loss of sodium in urine. Despite the natriuresis, in only 2 of 15 experiments did sheep drink significant amounts of .5 M NaCl solution during the first 10 hr after the onset of furosemide treatment, and hemoconcentration and arterial hypotension were evident during this time. By 24 hr, however, the saline consumption in all but three experiments had increased and compensated adequately (together with the water intakes) for the furosemide-induced loss of sodium-rich fluid in urine. These results provide evidence that following acute hypovolemia in sheep, as in rats, the onset of sodium appetite is delayed relative to the appearance of thirst.