Abstract
To determine whether chloride-depletion metabolic alkalosis (CDA) can be corrected by provision of chloride without volume expansion or intranephronal redistribution of fluid reabsorption, CDA was produced in Sprague-Dawley rats by peritoneal dialysis against 0.15 M NaHCO3; controls (CON) were dialyzed against Ringer's bicarbonate. Animals were infused with isotonic solutions containing the same Cl and total CO2 (tCO2) concentrations as in postdialysis plasma at rates shown to be associated with slight but stable volume contraction. During the subsequent 6 h, serum Cl and tCO2 concentrations remained stable and normal in CON and corrected towards normal in CDA; urinary chloride excretion was less and bicarbonate excretion greater than those in CON during this period. Micropuncture and microinjection studies were performed in the 3rd h after dialysis. Plasma volumes determined by 125I-albumin were not different. Inulin clearance and fractional chloride excretion were lower (P less than 0.05) in CDA. Superficial nephron glomerular filtration rate determined from distal puncture sites was lower (P less than 0.02) in CDA (27.9 +/- 2.3 nl/min) compared with that in CON (37.9 +/- 2.6). Fractional fluid and chloride reabsorption in the proximal convoluted tubule and within the loop segment did not differ. Fractional chloride delivery to the early distal convolution did not differ but that out of this segment was less (P less than 0.01) in group CDA. Urinary recovery of 36Cl injected into the collecting duct segment was lower (P less than 0.01) in CDA (CON 74 +/- 3; CDA 34 +/- 4%). These data show that CDA can be corrected by the provision of chloride without volume expansion or alterations in the intranephronal distribution of fluid reabsorption. Enhanced chloride reabsorption in the collecting duct segment, and possibly in the distal convoluted tubule, contributes importantly to this correction.