title: Renal acid-base excretion in normotensive salt-sensitive humans.
abstract: Reduced extracellular pH and bicarbonate levels recently have been reported in normotensive salt-sensitive 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 < .01) diets.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Internal Medicine, Free University of Berlin, FRG.
authors.forename: A M
authors.initials: AM
authors.lastname: Sharma
authors.forename: C
authors.initials: C
authors.lastname: Cetto
authors.forename: U
authors.initials: U
authors.lastname: Schorr
authors.forename: K P
authors.initials: KP
authors.lastname: Spies
authors.forename: A
authors.initials: A
authors.lastname: Distler
mesh_terms: D000136:Acid-Base Equilibrium; D000328:Adult; D000643:Ammonium Chloride / Q000494:pharmacology; D000704:Analysis of Variance; D001639:Bicarbonates / Q000097:blood / Q000652:urine; D001794:Blood Pressure / Q000187:drug effects*; D002951:Citrates / Q000494:pharmacology; D019343:Citric Acid; D006801:Humans; D006863:Hydrogen-Ion Concentration; D006973:Hypertension / Q000235:genetics / Q000503:physiopathology*; D007444:Inulin / Q000378:metabolism; D007668:Kidney / Q000502:physiology*; D008297:Male; D008657:Metabolic Clearance Rate; D016037:Single-Blind Method; D012964:Sodium / Q000652:urine; D017673:Sodium Chloride, Dietary / Q000494:pharmacology*; D014556:Urine / Q000737:chemistry*
chemical_list: D001639:Bicarbonates; D002951:Citrates; D017673:Sodium Chloride, Dietary; D000643:Ammonium Chloride; D019343:Citric Acid; D007444:Inulin; D012964:Sodium