Methods

Twenty normal subjects and 20 patients with chronic renal disease were studied. The normal subjects included six females and 14 males, ranging in age from 22 to 60 years (mean, 42 3 years, sEM). All were normal volunteers with a blood pressure consistently below 140/90 mm Hg. The patients includ-ed seven females and 13 males, ranging in age from 22 to 67 years (mean, 41 3 years). The diagnosis of renal disease, based on clinical signs, laboratory tests, and, in 11 patients, renal biopsy findings, was chronic glomerulonephritis in II patients; chronic pyelonephritis, interstitial nephritis of various etiology, and nephroangiosclerosis in two patients each; bilater-al hydronephrosis, reflux nephropathy in one patient each; and unclear in the last patient who had experienced an episode of acute oliguric renal failure (acute tubular necrosis) 3 years previously and since had mildly increased plasma creatinine levels. All patients were clinically stable and without signs of congestive heart failure or edema. To avoid very low or high sodium intakes, all subjects were instructed to adhere to their usual diet but not to add salt to their food during the study period [181. Antihypertensive drugs were discontinued 2 to 4 weeks before study. The following procedures were performed. Twenty-four-hour urinary sodium and potassium excretion rates, plasma sodium, potassium and creatinine, blood volume and exchangeable sodium were deter-mined, and plasma renin activity, aldosterone, norepinephrine (NE) and epinephrine levels, blood pressure and heart rate were measured after 1 hr of recumbency and again after 1 hr of ambulation, according to our standard procedure [191. One to five days later, the cardiovascular pressor reactivity to pressor doses of NE or angiotensin II (All) was determined, as de-scribed previously from this laboratory [20, 211. Basal (pre-infusion) levels of blood pressure, heart rate, plasma NE, and renin activity were determined after a 60-mm equilibration period with slow intravenous infusion of 5% dextrose solution in the supine position. The blood samples were collected between 9 and 11 AM An infusion of 1-NE or All (Hypertensin, Ciba, Basel, Switzerland) was then started and dosages were titrated to reach two target levels of mean (NE infusion) or diastolic (All infusion) blood pressure, namely 10 to 15 mm Hg (step 1) and 20 to 30mm Hg (step 2) above basal blood pressure.

Blood pressure was measured using standard cuff and sphyg-manometer; each recorded pressure was the mean of three measurements. Mean blood pressure was calculated as the sum of the diastolic (phase V) and one third of the pulse pressure. For determination of cardiovascular pressor reactivity, blood pressure was registered with the automatic recorder Physio-metrics SR 2. Plasma and urinary sodium and potassium concentrations were determined by flame photometer, creatinine by autoanalyzer. Blood volume and exchangeable sodium