“…The results Hypertension show a dichotomy between the enhanced fractional sodium excretion in the hypertensive subjects and the fractional phosphate excretion, which tended to be lower in this group than in normotensive subjects. These findings suggest an alteration of distal sodium reabsorption as the cause of the 'exaggerated' natriuresis of hypertensive subjects following saline infusion.Acute extracellular volume expansion (ECVE) has been shown to cause increased urinary phosphate excretion in both experimental animals and man [6,9,12,14], The mechanism of the phosphaturia following ECVE is still contraversial: in the dog, ECVE enhances phosphate excretion independently of changes in glomerular filtration rate (GFR) and parathyroid activity [8,9,14]; in rats, however, phosphate diuresis is almost abolished by parathyroid ectomy [6].It is well known that following ECVE with saline solutions, patients with essential hypertension react with an 'exaggerated' natriuresis as compared to similarly treated normotensive subjects [3][4][5]7]. In a recent study, hypertensive subjects were also shown to have an increased calcium excretion in response to saline loading [1],…”