Renal acid-base excretion in normotensive salt-sensitive humans.

Abstract

Reduced extracellular pH and bicarbonate levels recently have been reported in normotensive saltsensitive subjects. To assess the possible role of altered renal acid-base handling in the perturbation of acid-base status in these individuals, we measured the renal acid-base excretion after an acute oral administration of either an alkali or acid load in normotensive salt-sensitive and salt-resistant men. Twenty-four young (22 to 29 years old), healthy male volunteers were placed on a low-salt diet (20 mmol NaCl per day) for 2 weeks with either 220 mmol NaCl or placebo added to the low-salt diet for 1 week each in a randomized single-blind crossover order. Salt sensitivity was defined as a significant drop in mean arterial pressure (>3 mm Hg, mean of 60 readings taken on the seventh day of each diet, P<.05) during the low-salt diet 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 hours thereafter. According to the above definition, 13 subjects were considered salt sensitive. During the high-salt diet, mean arterial pressure was higher in the salt-sensitive than in the salt-resistant group (P<.01). Cumulative urinary bicarbonate excretion after the administration of sodium citrate was lower in the salt-sensitive than in the salt-resistant subjects during both the low-salt (46%, P<.001) and high-salt (32%, P<.0\) diets. Fractional sodium and bicarbonate excretion based on inulin clearance were likewise significantly lower in the salt-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 different between the two groups. Our finding of an enhanced bicarbonate reabsorption in salt-sensitive men could indicate a compensatory renal adaptation to metabolic acid overproduction. This perturbation of renal bicarbonate excretion may contribute to sodium retention and thus salt sensitivity in genetically susceptible humans. (Hypertension. 1993^22:884-890.) KEY WORDS • hypertension, sodium-sensitive • acid-base equilibrium • sodium • ammonium chloride • ion exchange • metabolism • diet, sodium-restricted

Salt-sensitive men show reduced heart rate variability, lower norepinephrine and enhanced cortisol during mental stress

“…5,6,21 Subjects received a standardized low-salt diet containing 20 mmol sodium, 20 mmol chloride, 60 mmol potassium and 20 mmol calcium per day for 14 days. To this diet, a daily supplement of 22 tablets of Slow Sodium (10 mmol NaCl per tablet; CIBA-GEIGY, Horsham, UK) and placebo were each given in a randomized single-blind crossover fashion for 7 days.…”

“…At the end of each week, after a 30 min resting period, BP was measured for assessment of SS in the recumbent position during 1 h at 1-min intervals with an automatic oscillometric device (DINAMAP 1846SX; Critikon). As in previous studies 5,6 SS was defined as a significant decrease in mean arterial pressure (MAP)43 mm Hg under the low-salt diet calculated as the difference between the average of the 60 readings under the high-and low-salt periods.…”

Association between the serum anion gap and blood pressure among patients at Harvard Vanguard Medical Associates

“…(interquartile range, 9-13; 5th-95th percentile, [6][7][8][9][10][11][12][13][14][15][16] Tables 1 and 2.…”

“…5 These same investigators also demonstrated that urinary bicarbonate excretion among salt-sensitive compared to salt-resistant individuals was 32 and 46% lower in response to an oral citrate load on fixed high-salt and low-salt diets, respectively. 6 The authors hypothesized that these findings could be explained as a compensatory mechanism to increased endogenous acid production among saltsensitive individuals. 6 Among more than 3000 participants of three large cohort studies (Nurses' Health Study 1, NHS1; Nurses' Health Study 2, NHS2; Health Professionals' Follow-up Study, HPFS), the adjusted odds ratios for prevalent hypertension among participants in Hypocitraturia (o320 mg day À1 ) was associated with significant 2.4-2.8-fold higher odds of prevalent hypertension in these cohorts.…”

“…6 The authors hypothesized that these findings could be explained as a compensatory mechanism to increased endogenous acid production among saltsensitive individuals. 6 Among more than 3000 participants of three large cohort studies (Nurses' Health Study 1, NHS1; Nurses' Health Study 2, NHS2; Health Professionals' Follow-up Study, HPFS), the adjusted odds ratios for prevalent hypertension among participants in Hypocitraturia (o320 mg day À1 ) was associated with significant 2.4-2.8-fold higher odds of prevalent hypertension in these cohorts. Urinary citrate excretion is regulated by systemic acid-base status, such that systemic acidosis and thus decreases in the intracellular pH of renal proximal tubular cells leads to decreases in urinary citrate.…”