Decreased renal tubular reabsorption of sodium in response to increased renal artery perfusion pressure, or "pressure natriuresis", has been demonstrated directly in animal experiments but not in man. In bilateral or single-kidney renovascular hypertension, hypertension has been attributed to reduced pressure natriuresis, and a similar mechanism may operate in chronic renal failure. We report a patient who presented with bilateral renovascular disease and was treated initially by unilateral nephrectomy. At a second operation the remaining ischemic kidney was revascularised. There followed a dramatic natriuresis, sufficient to cause clinical and biochemical features of hypovolemia. However, despite the natriuresis, systemic blood pressure remained elevated in the few weeks following surgery. We attribute the natriuresis to increased renal artery perfusion pressure, and conclude that acute pressure natriuresis sufficient to over-ride neurohormonal antinatriuretic mechanisms does occur in man. However, the failure to normalize blood pressure acutely following the natriuresis suggests that decreased sodium excretion is not the only mechanism which maintains hypertension in this unusual syndrome.