1963
DOI: 10.1172/jci104700
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Effect of Acute Metabolic Acidosis and Alkalosis on Acetate and Citrate Metabolism in the Rat*

Abstract: An enhanced urinary excretion of citrate after administration of alkali and a diminished citrate excretion after administration of ammonium chloride were first observed by Ostberg in 1931 (1). More recently, it has been pointed out that the quantity of citrate excreted in the urine is not a direct consequence of acidification or alkalinization of the urine as believed by Ostberg, but rather is related to systemic pH (2). Hypercitraturia is associated with alkalosis and hypocitraturia with acidosis. This correl… Show more

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Cited by 23 publications
(9 citation statements)
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“…The normal kidney tissue citrate (KT,,,) levels in the present study agree well with those of Crawford, Milne & Scribner (1959) and Gordon (1963). KTcit was significantly elevated above the normal by acetazolamide treatment (Table 2) and the group receiving diet B plus acetazolamide had the highest content of kidney tissue calcium and also the highest content of kidney tissue citrate.…”
Section: Kidney Tissue Valuessupporting
confidence: 92%
“…The normal kidney tissue citrate (KT,,,) levels in the present study agree well with those of Crawford, Milne & Scribner (1959) and Gordon (1963). KTcit was significantly elevated above the normal by acetazolamide treatment (Table 2) and the group receiving diet B plus acetazolamide had the highest content of kidney tissue calcium and also the highest content of kidney tissue citrate.…”
Section: Kidney Tissue Valuessupporting
confidence: 92%
“…With diet-dependent chronic metabolic acidosis, renal and extrarenal homeostatic adaptations occur that serve to minimize disturbances in [H ϩ ] b and [HCO] p , but these adaptations themselves are detrimental. Those include decreased renal citrate production and excretion (27), hypercalciuria (28), dissolution of bone (29), protein catabolism and muscle wasting (1-3), and progression of renal disease (30). Thus, homeostatic mitigation of the disturbance of extracellular acid-base equilibrium requires the body to accept certain deleterious trade-offs (26).…”
Section: Discussionmentioning
confidence: 99%
“…Thus, in different models of alkalosis in the rat, no redistribution of intranephronal fluid reabsorption has been detected and, at least in the rat, recovery from CDA can proceed without such adjustments. Metabolic alkalosis may stimulate the production and excretion of other organic anions (40,41), alter intestinal anion transport (42), and lead to shifts in anions between extracellular and intracellular spaces (43). Our studies do not address these possible extrarenal homeostatic mechanisms but on the basis of our estimates of plasma volume, net intercompartmental fluid shifts do not appear to participate detectably in the correction of plasma anion composition.…”
Section: Discussionmentioning
confidence: 83%