The study was designed to determine to which extent moderate elevation of renal perfusion pressure (RPP) via the mechanism of "pressure natriuresis" contributes to the natriuresis induced by acute i.v. saline loading. Nine Beagle dogs maintained on ample sodium intake (5.5 mmol per kg body mass per day) were chronically equipped with an aortic occluder to servocontrol RPP, a bladder catheter to measure renal function, and catheters for measurement of RPP and mean arterial blood pressure (MABP). A swivel system allowed free movement in the kennel during experiments. Isotonic saline loading (500 ml in 100 min) was studied in 4 protocols: with and without servocontrol of RPP, and with and without angiotensin converting enzyme inhibition (ACEI, Enalapril, 2 mg/kg body mass). Saline loading increased MABP by about 12 mmHg and sodium excretion from about 28 µmol/min up to about 350 µmol/min. Without ACEI, servocontrol of RPP at 10% below control 24-h MABP slightly delayed the onset of the saline-induced natriuresis, but did not reduce peak sodium excretion or cumulative sodium excretion. The slight delay most probably resulted from pressure-controlled renin release because with ACEI, servocontrol of RPP did not delay nor reduce the saline-induced natriuresis. In conclusion, pressure natriuresis does not contribute to the natriuresis following acute saline loading.