Effects of K‐deficient diets ± Na supplementation on Na, K, and H 2 O transporters’ abundance along the nephron

Previous studies of K deficiency compared chow with 2% KCl, 0.74% NaCl ( 2K1Na ) to K deficient chow: 0.03% KCl, 0.74% NaCl ( 0K1Na ). We tested whether previously reported responses to 0K diet are due to low electrolytes, rather than hypokalemia. SD rats were fed 6 d with gelled diet prepared from powdered base adjusted to 2K1Na, 0K1Na, and with added NaCl: 2% KCl, 2% NaCl ( 2K2Na) and 0.03% KCl, 2% NaCl ( 0K2Na). Abundance was assessed by immunoblot of homogenates, densities normalized to mean of 2K groups. Results 1) In both 0K groups, plasma K fell to 2.5 mM, urine K fell to < 10 μmol/hr and outer medulla hypertrophied. 2) The only differences seen in both 0K groups are: ↓cortex ENaC and ↑medulla Na,K‐ATPase (NKA). 3) The following changed in 0K1Na but not 0K2Na: ↑cortex gastric H,K‐ATPase (HKA), ↑medulla NHE3, NHE3‐P and ↓AQP2. 4) In 0K2Na but not 0K1Na: cortex SPAK and OSR1 ↑ despite lowest plasma aldo in 0K2Na (172 pg/ml) vs. 0K1Na (413 pg/ml) and 2K2Na (417 pg/ml) and with no changes in NCC‐P or NKCC‐P. Conclusions Despite profound hypokalemia and low urinary K, previously reported changes with 0K diets (↑NHE3, ↓NKCC, ↓NCC, ↓ROMK, ↑c‐Src, ↑HKA, ↓AQP2) were not observed; some may be secondary to low electrolytes. ↓ENaC can decrease driving force for K secretion, and ↑NKA is secondary to hypertrophy. Changes in transporter distribution and activity appear more important for conserving K than changes in abundance. DK0837854