Mechanism of NaCl reabsorption and glomerulotubular balance in hyperchloraemic acidosis

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Abstract
To elucidate the mechanism of reduced NaCl reabsorption during hyperchloraemic acidosis, experiments were performed in anaesthetized dogs before and after intravenous infusion of HC1 until plasma bicarbonate concentration averaged 8.9±1.0 mmol/l. Ethacrynic acid was infused to inhibit transcellular NaCl reabsorption and impair autoregulation. Perfusion pressure was altered by aortic and carotid constriction permitting variations in glomerular nitration rate (GFR) between 25 and 150% of control. Glomerulotubular balance, denned as the ratio of change in reabsorption and GFR, was reduced by hyperchloraemic acidosis for bicarbonate from 18±1 to 7±1 μmol per ml GFR, for chloride from 60±2 to 39±2 μmol per ml GFR and for sodium from 89±4 to 59±3 μmol per ml GFR. Glomerulotubular balance applied up to a GFR of 150% during hyperchloraemic acidosis, whereas maximal reabsorption rates were reached at control GFR when plasma bicarbonate concentration was normal. After complete inhibition of carbonic anhydrase by acetazolamide (500 mg/kg body wt), glomerulotubular balance was maintained up to 75% of control GFR during hyperchloraemic acidosis. On average, about 2 mol NaCl were reabsorbed for each mole NaHCO3. To conclude, inhibition of NaCl reabsortion and altered glomerulotubular balance during hyperchloraemic acidosis is due to reduced plasma concentration of bicarbonate so that the reabsorptive capacity for bicarbonate is approached first at high GFR. Because of reduced bicarbonate reabsorption the reabsorption of water and NaCl through the tight junction is reduced.

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