The goal of this study was to quantitate changes in mean arterial pressure (MAP) and renal function during chronic increases in plasma levels of norepinephrine, and to determine the role of the renal pressure natriuresis mechanism in controlling sodium balance in norepinephrine hypertension. In six conscious dogs in which renal artery pressure (RAP) was allowed to increase during 7 days of norepinephrine infusion (0.2 .mu.g/kg per min), sodium excretion (uNAV) rose from 66 .+-. 3 to 112 .+-. 15 mmol/day and MAP increased from 100 .+-. 3 to 109 .+-. 3 mmHg on the first day. On days 2-7, UNaV returned toward the control level while MAP averaged 108 .+-. 2 mmHg. Glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) did not change significantly, averaging 85.9 .+-. 4.0 and 235 .+-. 17 ml/min, respectively, during 7 days of norepinephrine, compared to controls of 84.1 .+-. 3.9 and 252 .+-. 20 ml/min. When RAP was servo-controlled for 7 days during norepinephrine infusion, the natriuresis was abolished; UNaV averaged 76 .+-. 8 during control, 77 .+-. 13 during the first day of norepinephrine and 65 .+-. 4 mmol/day during 7 days of norepinephrine. GFR and ERPF did not change significantly during norepinephrine infusion with RAP held constant. MAP did not reach a plateau but continued to rise from 102 .+-. 3 to 137 .+-. 3 mmHg after 7 days of norepinephrine and servo-control of RAP. When servo-control of RAP was stopped while norepinephrine infusion was continued for 7 days, uNAV increased to 120 .+-. 13 mmol/day on the first day and MAP decreased to 125 mmHg. These data indicate that in normal dogs, chronic increases in plasma norepinephrine produce mild hypertension associated with sodium loss due to pressure natriuresis. However, when pressure natriuresis is impaired by servo-controlling RAP, the sodium loss is abolished and the hypertensive effects of norepinephrine are much more severe.