RENAL ACID-BASE EXCRETION IN NORMOTENSIVE SALT-SENSITIVE HUMANS

Reduced extracellular pH and bicarbonate levels recently have been rep orted in normotensive salt-sensitive subjects. To assess the possible role of altered renal acid-base handling in the perturbation of acid-b ase status in these individuals, we measured the renal acid-base excre tion after an acute oral administration of either an alkali or acid lo ad in normotensive salt-sensitive and salt-resistant men. Twenty-four young (22 to 29 years old), healthy male volunteers were placed on a l ow-salt diet (20 mmol NaCl per day) for 2 weeks with either 220 mmol N aCl or placebo added to the low-salt diet for 1 week each in a randomi zed single-blind crossover order. Salt sensitivity was defined as a si gnificant drop in mean arterial pressure (>3 mm Hg, mean of 60 reading s taken on the seventh day of each diet, P<.05) during the low-salt di et. On the fifth and seventh days of each week, subjects were given an oral load of either sodium citrate (0.7 mmol/kg) or ammonium chloride (2.2 mmol/kg), respectively, in a randomized order, and arterial and urinary acid-base status was assessed at baseline and followed for 8 h ours thereafter. According to the above definition, 13 subjects were c onsidered salt sensitive. During the high-salt diet, mean arterial pre ssure was higher in the salt-sensitive than in the salt-resistant grou p (P<.01). Cumulative urinary bicarbonate excretion after the administ ration of sodium citrate was lower in the salt-sensitive than in the s alt-resistant subjects during both the low-salt (46%, P<.001) and high -salt (32%, P<.01) diets. Fractional sodium and bicarbonate excretion based on inulin clearance were likewise significantly lower in the sal t-sensitive individuals after sodium citrate intake during both diets (P<.05), pointing to increased sodium and bicarbonate reabsorption. In contrast, net acid excretion after ammonium chloride was not differen t between the two groups. Our finding of an enhanced bicarbonate reabs orption in salt-sensitive men could indicate a compensatory renal adap tation to metabolic acid overproduction. This perturbation of renal bi carbonate excretion may contribute to sodium retention and thus salt s ensitivity in genetically susceptible humans.