Abstract
During infusions of 5% dextrose in water urinary sodium excretion and the renal tubular rejection of filtered sodium (E/F Na %) were significantly higher in hypertensive than in normotensive subjects. Increased E/F Na % did not result from alterations in plasma sodium, in filtered sodium, or from an osmotic diuresis. Fractional sodium reabsorption in proximal (isosmotic) portions of the nephron was diminished in the hypertensive patients. Free water formation (C H H2 o rose with increased "distal" sodium delivery (V) in both groups; however, fractional sodium reabsorption in the "distal" nephron was significantly impaired in the hypertensive patients and urinary osmolality was increased. Mean arterial blood pressure and E/F Na % were related in curvilinear fashion in the 31 studies, and there was a direct relation between E/F Na % and the magnitude of renal vascular resistance. The data suggested that alterations of renal arterial pressure and vascular resistance in hypertensive disease modify sodium transport in proximal and diluting segments of the nephron and determine to a major extent the increased natriuresis exhibited by hypertensive subjects during infusions that expand extracellular fluid volume.