Decreased renal tubular reabsorption of sodium in response to increase
d renal artery perfusion pressure, or ''pressure natriuresis'', has be
en demonstrated directly in animal experiments but not in man. In bila
teral or single-kidney renovascular hypertension, hypertension has bee
n attributed to reduced pressure natriuresis, and a similar mechanism
may operate in chronic renal failure. We report a patient who presente
d with bilateral renovascular disease and was treated initially by uni
lateral nephrectomy. At a second operation the remaining ischemic kidn
ey was revascularised. There followed a dramatic natriuresis, sufficie
nt 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 incr
eased renal artery perfusion pressure, and conclude that acute pressur
e natriuresis sufficient to over-ride neurohormonal antinatriuretic me
chanisms does occur in man. However, the failure to normalize blood pr
essure acutely following the natriuresis suggests that decreased sodiu
m excretion is not the only mechanism which maintains hypertension in
this unusual syndrome.