Abstract

To examine the characteristics of transcellular, energy-requiring NaCl reabsorption, increased delivery of tubular fluid of different bicarbonate and chloride composition to the outer medulla was achieved by infusion of acetazolamide (30 mg/kg body wt) or 0.9% NaCl in anaesthetized dogs. As an index of energy-requiring NaCltransport, cortical and outer medullary metabolism were determined by the heat production technique. Outer medullary metabolism was correlated to sodium excretion but not to chloride excretion. A rise in sodium excretion up to 20-25% of the filtered load during hydropenia was associated with a 70-80% increase in outer medullary metabolism. Further increments in sodium excretion induced by increasing systemic blood pressure and thereby increasing glomerular filtration rate or by infusing 2.9% NaCl did not significantly increase either reabsorption of sodium or cortical and outer medullary metabolism. By infusion of furosemide (2mg/kg body wt) sodium reabsorption and outer medullary heat production could be reduced below control values. These experiments show that sodium rather than chloride determine transcellular NaCl reabsorption. The maximal capacity of this reabsorption system is approached first at sodium excretion rates beyond the physiological range. Calculations based on clearance studies and heat production measurements, before and after furosemide infusion, indicate that transcellular NaCl reabsorption accounts for more than half of the NaCl reabsorption in the kidney.

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