(Na+,K+)-ATPase kinetics within the intact renal cell. The role of oxidative metabolism.
The kinetics of oxygen consumption and (Na+,K+)-ATPase-mediated K+ transport was examined by reintroducing K+ into a K+-depleted suspension of renal tubules. In the presence of the substrates glucose, lactate, and alanine, a K+/O2 ratio of 10.4 +/- 0.2 was obtained, and the apparent K1/2 for K+ transport with respect to external K+ concentration was 0.9 mM. Supplementation of the substrates with the short chain fatty acid, butyric, had a 3-fold effect on the kinetic parameters examined: 1) the quantity of (Na+,K+)-ATPase-mediated ion transport per oxygen consumed fell by 17 +/- 2%; 2) the maximum rate of K+ transport increased by nearly 50%; and 3) the apparent K1/2 for transport with respect to external K+ concentration rose to 1.5 mM. These results indicate that despite decreasing the quantity of ATP produced per oxygen consumed, short chain fatty acids are able to increase the overall production of ATP during periods of high metabolic demand. The coupling between the two major metabolic processes of the renal cell, (Na+,K+)-ATPase-mediated ion transport and mitochondrial oxidative phosphorylation, is addressed in the context of these findings.
D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D007672:Kidney Cortex / Q000378:metabolism*; D007684:Kidney Tubules / Q000378:metabolism; D007700:Kinetics; D010101:Oxygen Consumption / Q000187:drug effects; D011188:Potassium / Q000378:metabolism / Q000494:pharmacology; D011817:Rabbits; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*
D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium