1. This study aims at determining whether elevation of renal perfusion pressure (RPP) may correct for increased total body sodium (TBS), via pressure natriuresis. 2. Freely moving dogs were studied on four consecutive days. During day 1, low-dose angiotensin II and aldosterone were infused. Pressure natriuresis was prevented by servo-controlling RPP to 20 % below the control level. Sodium and water retention increased TBS and total body water. Mean arterial blood pressure rose by approximately 25 mmHg. 3. In protocol 1, infusions and control of RPP were maintained over three more days. Sodium was retained on all days, resulting in a continuous increase in TBS. 4. In protocol 2, control of RPP was stopped after day 1. Thus, pressure natriuresis could exert its effect beginning with day 2. Angiotensin II and aldosterone infusions were continued. This prevented the effects of endogenous suppression of the renin-angiotensin-aldosterone system (RAAS), which is caused by increased TBS. No further sodium retention occurred, i.e. TBS remained at the elevated level gained on day 1. 5. In protocol 3, control of RPP and the infusions were stopped. Thus, pressure natriuresis and RAAS suppression could exert their combined effects. Sodium excretion exceeded sodium intake on day 2. Control level of TBS was regained within 24 h. 6. It was concluded that when RPP is considerably elevated, pressure natriuresis prevents further increase of TBS in the face of elevated angiotensin II and aldosterone levels. However, pressure natriuresis does not suffice to restore TBS to control. This requires additional endogenous suppression of RAAS.