1. In order to investigate the mechanisms of hypovolaemic thirst and sodium appetite an inflatable balloon in the upper abdominal inferior vena cava was used to produce acute, graded and reversible reductions in venous return to the heart in conscious dogs. 2. Reducing venous return caused a fall in central venous, arterial and pulse pressures. Heart rate and venous pressure upstream from the point of inflation rose. 3. Within 6--28 min of inflating the balloon the dogs started drinking. The amount drunk in a 1 h experiment was significantly correlated with the changes in central venous and arterial pressures. 4. More prolonged obstruction to venous return led to a sustained increase in water intake and the development of a sodium appetite. 5. Plasma renin activity and concentration rose following caval obstruction. 6. Drinking in response to reductions in venous return was reduced, but not abolished, by simultaneous infusion of the competitive angiotensin II antagonist saralasin acetate. 7. When the left vagosympathetic nerve was blocked at the same time as balloon inflation the response was enhanced. 8. Urine flow fell after partial obstruction of the vena cava. Therefore drinking led to the development of a positive fluid balance. 9. We have shown that hypovolaemia is a potent and quantitatively defined stimulus to drinking in the dog and that the renal renin-angiotensin system makes an important contribution to it.