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School of Physiology and Pharmacology, University of New South Wales, Sydney, Australia.

1. The effects of I.V. infusions of 6.7-19.3 mmol hydrochloric acid/kg on fetal renal function were studied in fourteen chronically catheterized fetal sheep aged 121-143 days. Infusion of acid caused arterial pH and plasma bicarbonate levels to fall (P less than 0.0005, P less than 0.001). These remained low for the next 3 h. Plasma chloride levels increased (P less than 0.0005). There were no other changes in plasma electrolytes nor in plasma osmolality. 2. Fetal glomerular filtration rate did not change; the fractional reabsorptions of sodium, chloride and phosphate all decreased (P less than 0.005). Initially urine volume did not change but urinary osmolality increased (P less than 0.0005). Fetal urinary pH fell abruptly, titratable acid excretion increased, urinary ammonium excretion increased (P less than 0.0005) but urinary bicarbonate excretion remained unchanged. Thus, net acid excretion increased significantly (P less than 0.0005). 3. Twenty-six hours after infusion of acid, fetal arterial pH, bicarbonate levels, urinary pH, titratable acid and ammonium excretion were no different from control. Net acid excretion was still increased (P less than 0.05), urine flow rate was less (P less than 0.01) and urinary osmolality still increased (P less than 0.05). 4. There were no differences in arterial blood gases nor in pH of four fetuses which died during or shortly after infusion of acid. However, prior to acid infusion they were already excreting significantly greater amounts of phosphate (P less than 0.01), ammonium and titratable acid (P less than 0.02). Thus the fetal kidney responds to a metabolic acidosis by excreting more acid and by generating more bicarbonate, but this response is limited.

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