Energy source for transepithelial sodium transport in rat renal proximal tubules.

Abstract

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.