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.