Effects of potassium depletion on renal tubular chloride transport in the rat

Effects of potassium depletion on renal tubular chloride transport in the rat. Potassium depletion (KD) causes renal chloride-wasting. To investigate the effects of KD on renal tubular reabsorption of chloride, balance, clearance, micropuncture, and microinjection studies were performed on potassium-depleted rats. KD was produced by omitting potassium from the diet and by administration of DOC A on days 2 and 3; rats were studied on days 9 to 12. Diets were chloride-free in both control and KD groups. In the KD group, balance experiments confirmed greater chloride depletion and continued chloride-wasting, and clearance studies showed an increased FECl. Muscle potassium was reduced by 27% as compared to control. Whole kidney and single nephron GFR were reduced in KD rats to 72 and 74% of control. Fractional (6 ± 6% vs. 22 ± 4%, P < 0.05) and absolute chloride reabsorption in the proximal tubule were reduced in KD, and chloride delivery out of the proximal tubule was not different. Fractional reabsorption of delivered chloride was reduced in the loop of Henle (92 ± 0.8% in KD vs. 95 ± 0.7% in control, P < 0.02). Transtubular chloride ratio (0.28 ± 0.02 vs. 0.21 ± 0.02, P < 0.02) was increased at the early distal tubule. Fractional delivery of chloride (8 ± 0.9 vs. 5 ± 0.5%, P < 0.02), and fluid (26 ± 1 vs. 22 ± 1%, P < 0.05) were also increased in KD at the early distal tubule. Recovery of chloride 36 injected into late distal tubules was 88 ± 1% on a normal chloride intake, 62 ± 2% in chloride depletion, and 88 ± 2% in potassium and chloride depletion. Thus, KD depresses chloride reabsorption in the proximal tubule and in the loop of Henle, and it decreases chloride 36 efflux from the collecting duct