Chloride depletion and hypochloraemia as a cause of renal sodium and water loss in the rat.

1. To study the effects of chloride depletion, without sodium depletion or change in plasma tonicity, on renal excretion of sodium and water, a single exchange peritoneal dialysis was performed in rats against a solution of glucose (15 g/1) containing either NaCl (150 mmol/l, control) or NaHCO3 (150 mmol/l, experimental); KHCO3 (4mmol/l)was added to both solutions. All rats were prepared before dialysis by a low NaCl diet for 10 days. 2. Peritoneal dialysis against NAHCO3 consistently produced a negative sodium and water balance compared with dialysis against NaCl. Despite this, subsequent electrolyte balance for 3 days showed that chloride-depleted rats excreted significantly more sodium and water and had a reduced urinary osmolality as compared with control animals. Increased sodium and water loss were unexplained by osmotic or bicarbonate diuresis. Kaliuresis was seen in the chloride-depleted rats but muscle potassium was not significantly depressed. 3. With sodium and water loss and continued renal chloride conservation, plasma chloride rose on the average from 88 mmol/l after dialysis against NaHCO3 to 100 mmol/l (control 104 mmol/l) at 72 h. Concomitant with this increase in plasma [C1-], on the third day after dialysis, during hydropenia, urinary osmolality and papillary [Na+] were not different from control cencentrations. 4. It is postulated that chloride depletion and/or hypochloraemia leads to diminished chloride transport in the loop of Henle and that this causes reduced sodium transport into the medulla, impaired concentration ability and inappropriate urinary sodium loss.