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Sodium Reabsorption; Oxidative Phosphorylation; Metabolic Inhibitors; Na+−K+ ATPase; Exogenous Energy Supply; Carrier Albumin
Abstract:
The effects of various metabolic inhibitors on isotonic fluid absorption (JV) 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 (5×10−5M, 10−4M) and Antimycin A (10−5M, 10−4M) 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 10−5M Antimycin A when the Na+−K+ ATPase inhibition was apparently small.
The uncoupler, carbonyl cyanide m-chlorophenyl hydrazone (CCCP) (10−3M), as well as sodium cyanide (5×10−3M) inhibited JV 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.
