Influence of plasma potassium concentration on the capacity for sodium reabsorption in the diluting segment of the kidney

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Abstract
A previous study showed that sodium reabsorption and heat production in the outer medulla and cortex increased during saline loading until 15-20% of the filtered sodium was excreted. To examine if the capacity for energy-requiring transcellular sodium reabsorption is altered by changes in plasma potassium concentration, renal heat production and sodium reabsorption were measured in anaesthetized dogs during hypokalemia, normokalemia and hyperkalemia. A rise in plasma potassium concentration from 1.8 to 4 mmol/l was associated with a 50% increase in both outer medullary heat production and sodium reabsorption in dogs which received acetazolamide to avoid changes in proximal tubular reabsorption; cortical metabolism increased only slightly. In contrast, no change in tubular reabsorption of sodium was observed during intravenous infusion of KC1 to hypokalemic dogs which had not received acetazolamide. Under this condition an increase in sodium reabsorption in the diluting segment is counteracted by a reduction in proximal tubular reabsorption because of reduced plasma bicarbonate concentration. A rise in plasma potassium concentration from normokalemic levels to 6-8 mmol/l had no effect on outer medullary heat production and sodium reabsorption. Thus potassium administration to normokalemic dogs has no natriuretic effect when GFR and plasma bicarbonate concentration are kept constant. During hypokalemia the capacity for trans-cellular sodium reabsorption in the diluting segment is reduced, as expected for Na-K-ATPase dependent transport. This defect can be immediately repaired by restoring normal potassium concentration.

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