Energy source for transepithelial sodium transport in rat renal proximal tubules

Summary The effects of various metabolic inhibitors on isotonic fluid absorption (J_V) in rat proximal tubules and on the Na⁺–K⁺-ATPase of isolated cell membranes of rat kidney cortex were investigated by the shrinking split oil droplet technique and biochemical methods respectively.Both Oligomycin (5×10^–5 M, 10^–4 M) and Antimycin A (10^–5 M, 10^–4 M) inhibited isotonic fluid absorption by 80% when applied intratubularly but only in conjunction with bovine serum albumin. At these concentrations they inhibited a Na⁺–K⁺ activated adenosine triphosphate phosphohydrolase (Na⁺–K⁺ ATPase E.C. 3.6.1.3.) of cell membranes isolated from rat kidney cortex by 77%, 82% and 55%, 95%, respectively.Sodium phosphoenolpyruvate (PEP) 5×10^–3 M could partially reverse the inhibition of the isotonic fluid absorption but only with 10^–5 M Antimycin A when the Na⁺–K⁺ ATPase inhibition was apparently small.The uncoupler, carbonyl cyanide m-chlorophenyl hydrazone (CCCP) (10^–3 M), as well as sodium cyanide (5×10^–3 M) inhibitedJ_V 100%, but only when applied through peritubular blood capillary perfusion.From these findings it was concluded thatall proximal tubular isotonic fluid absorption is supported by energy fromoxidative processes, and that in a least 80% of this sodium reabsorption, ATP from oxidative phosphorylation is directly involved, while, for the remaining 20% non ATP energy is responsible.C. J. Martin Fellow of the National Health and Medical Research Council of Australia.