Influence of the Renal Excretion of Sodium Chloride Upon the Renal Excretion of Magnesium and Other Ions by Human Subjects*

Ag, Hills; Dw, Parsons; Webster, Gregory D.; Rosenthal, Otto; H, Conover

doi:10.1210/jcem-19-10-1192

Cited by 50 publications

(20 citation statements)

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“…In vivo and in vitro experiments have demonstrated that alterations in urinary sodium excretion affect the renal handling of calcium [4][5][6][7][8][9]. A direct, proportional relationship has been reported [5][6][7][8][9] in studies that were limited to normal levels of sodium intake and, therefore, excretion.…”

Section: Discussionmentioning

confidence: 99%

“…The relationship between urinary sodium and calcium excre tion has been well characterized [4][5][6][7][8][9], Throughout the usual range of sodium intake, urinary calcium excretion (UcaV) increases in direct proportion to sodium excretion (UNaV), even when calcium intake is held constant [5][6][7][8][9][10]. Little, though, is known about chronic effects of excessive sodium intake on the renal handling of calcium [3].…”

Section: Introductionmentioning

confidence: 99%

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Urinary Calcium Excretion at Extremes of Sodium Intake in Normal Man

et al. 1981

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To elucidate the relationship between the renal regulation of sodium and calcium excretion at extremes of sodium intake, we studied 6 normal men ingesting a fixed, 400 mg/day calcium intake and four levels of sodium intake from 10 to 1,500 mEq/day. Serum ionized calcium was not influenced by sodium intake. Blood pressure and cardiac index increased modestly. Urinary calcium excretion increased to 262 ± 53 mg/day (mean ± SE). Plasma norepinephrine concentration, serum PTH levels, hematocrit, total serum protein concentrations and CO₂ content decreased with increasing sodium intake. Urinary cAMP increased as sodium intake was raised from 10 to 300 mEq/day, but subsequently decreased to basal values. Urinary calcium and sodium excretion were related (p < 0.001) in a nonlinear fashion as were the fractional excretions of these cations (p < 0.001). The filtered calcium load and the fractional calcium excretion were directly and linearly related (p < 0.001). We conclude that the effect of sodium intake on urinary calcium excretion principally reflects changes in the filtered calcium load rather than changes in renal sodium handling. Calcium homeostasis at extremes of sodium intake does not appear to be critically dependent upon PTH-mediated mechanisms. The data suggest that the proximal tubule has a remarkable capacity to dissociate calcium resorption from that of sodium.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Urinary Calcium Excretion at Extremes of Sodium Intake in Normal Man

et al. 1981

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“…We had observed previously that renal tubular calcium reabsorption was inhibited during stable experimental metabolic acidosis and that the increments in urinary calcium excretion during acidosis were closely correlated with simultaneous increments in urinary ammonium excretion (5). Increases in urinary magnesium excretion have also been found in some (6,7) but not all (8, 9) studies of experimental metabolic acidosis. We speculated about whether glucose ingestion and chronic metabolic acidosis might inhibit renal tubular divalent cation reabsorption by some common mechanism.…”

Section: Introductionmentioning

confidence: 85%

A comparison of the effects of glucose ingestion and NH4Cl acidosis on urinary calcium and magnesium excretion in man

Lennon¹,

Piering²

1970

J. Clin. Invest.

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“…Dietary sodium intake has long been known to influence urinary calcium excretion in man (Aub et al 1937;Hills et al 1959) and animals (Walser, 1961 ;Massry et al 1967). However, up to the early 1980s Na was not included among dietary factors believed to influence Ca requirements or the pathogenesis of osteoporosis (Draper & Bell, 1979;Spencer et al 1982).…”

Section: Introductionmentioning

confidence: 99%