AJP - Cell Physiology, Vol 256, Issue 4 C823-C830, Copyright © 1989 by American Physiological Society

ARTICLES

Cellular pathways of potassium transport in renal inner medullary collecting duct

B. C. Kone, D. Kikeri, M. L. Zeidel and S. R. Gullans
Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston 02115.

The dominant K+ transport pathways in rabbit inner medullary collecting duct (IMCD) cells were identified using an extracellular K+ electrode and fluorometric estimates of membrane potential. Ba2+ (5 mM) caused an initial rate of net K+ influx (61 +/- 6 nmol K+.min-1. mg protein-1) equivalent to the net K+ efflux (59 +/- 5 nmol K+. min-1.mg protein-1) induced by ouabain (0.1 mM). Addition of ouabain to Ba2+ -treated cells caused no net K+ flux. Membrane potential experiments demonstrated a K+ conductance that was inhibited by Ba2+. Thus K+ transport in the IMCD occurs principally via Ba2+ -sensitive K+ conductive pathway(s) and Na+-K+-ATPase. In studies that examine the metabolic determinants of K+ transport in the IMCD, glucose (but not 3-O-methylglucose) augmented oxygen consumption (QO2; + 12%) and cell K+ content (+12%), whereas iodoacetic acid, an inhibitor of glycolysis, promoted a release of cell K+. However, inhibition of mitochondrial oxidative phosphorylation with rotenone demonstrated that glycolysis alone could not maintain cell K+ content. Thus glucose metabolism plays an important role in K+ transport in the IMCD, but both glycolysis and oxidative phosphorylation are required to maintain optimal cellular K+ gradients.

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				A. M. Weinstein A mathematical model of the inner medullary collecting duct of the rat: pathways for Na and K transport Am J Physiol Renal Physiol, May 1, 1998; 274(5): F841 - F855. [Abstract] [Full Text] [PDF]