Clearance and micropuncture studies have been performed in dogs to examine the effects of acute and chronic metabolic acidosis and acute alkalosis on tubular sodium and calcium transport. Acute metabolic acidosis, induced by the infusion of hydrochloric acid, decreased proximal fluid reabsorption and increased the fractional delivery of sodium and calcium to the distal tubule, but not to the final urine. In comparison with normal dogs, dogs with chronic metabolic acidosis (induced by feeding ammonium chloride) showed an increase in proximal fluid reabsorption and a dissociation of calcium from sodium reabsorption more distally, leading to an increased delivery of calcium relative to sodium at the distal tubule and in the final urine. The infusion of sodium bicarbonate to correct chronic metabolic acidosis, both in intact and thyroparathyroidectomized (TPTX) dogs, reduced proximal fluid reabsorption and caused a selective enhancement of calcium reabsorption relative to sodium in the more distal nephron, resulting in a reversal of the dissociation observed in acidosis, both at the distal tubule and in the final urine. By contrastin fusion of sodium chloride in parathyroid-intact acidotic dogs did not reduce proximal fluid reabsorption or enhance tubular calcium reabsorption. In nonacidotic dogs, both intact and TPTX, infusion of sodium bicarconate to induce acute alkalosis resulted in selhese data demonstrate the presence of a component of tubular calcium reabsorption situated beyond the proximal tubule, which is inhibited by chronic (but not acute) metabolic acidosis and enhanced by metabolic alkalosis (or bicarbonate infusion) independently of parathyroid hormone.
Magnesium and calcium transport was studied in the superficial proximal tubule, loop of Henle, and superficial distal tubule of the rat by in vivo microperfusion. Magnesium chloride was used to vary plasma and perfusate magnesium concentration. Perfusion with magnesium-free Ringer solution resulted in little magnesium entry into the tubule lumen in either normomagnesemic or hypermagnesemic rats. Magnesium concentration increased with water abstraction along the perfused proximal tubule whether markedly above or below plasma concentrations. Absolute proximal magnesium reabsorption increased with perfusate concentration; however, fractional magnesium and calcium reabsorption decreased in proportion to net sodium reabsorption with elevated extracellular magnesium. Magnesium absorption increased in the loop of Henle proportional to luminal magnesium concentration. Sodium and calcium reabsorption was not affected. Acute elevation of plasma magnesium, however, significantly depressed absolute magnesium reabsorption to a greater degree than calcium whereas sodium was unchanged. The effects of extracellular magnesium onloop reabsorption were reflected in the final urine. Reabsorption of sodium, calcium, and magnesium in the perfused distal tubule was concentration-dependent and not altered by luminal or extracellular magnesium concentration.
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