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A mathematical model of rat distal convoluted tubule. II. Potassium secretion along the connecting segment

Department of Physiology and Biophysics Weill Medical College of Cornell University, New York, New York

Submitted 1 February 2005 ; accepted in final form 14 April 2005

A simulation of the rat distal convoluted tubule (DCT) is completed with a model of the late portion, or connecting tubule (CNT). This CNT model is developed by relying on a prior cortical collecting duct (CCD) model (Weinstein AM. Am J Physiol Renal Physiol 280: F1072–F1092, 2001), and scaling up transport activity of the three cell types to a level appropriate for DCT. The major difference between the two tubule segments is the lower CNT water permeability. In early CNT the luminal solution is hypotonic, with a K⁺ concentration less than that of plasma, and it is predicted that osmotic equilibration requires the whole length of CNT, to end with a nearly isotonic fluid, whose K⁺ concentration is severalfold greater than plasma. With respect to potassium secretion, early CNT conditions are conducive to maximal fluxes, whereas late conditions require the capacity to transport against a steep electrochemical gradient. The parameter dependence for K⁺ secretion under each condition is different: maximal secretion depends on luminal membrane K⁺ permeability, but the limiting luminal K⁺ concentration does not. However, maximal secretion and the limiting gradient are both enhanced by greater Na⁺ reabsorption. While higher CNT water permeability depresses K⁺ secretion, it favors Na⁺ reabsorption. Thus in antidiuresis there is a trade-off between enhanced Na⁺-dependent K⁺ secretion and the attenuation of K⁺ secretion by slow flow. When the CNT model is configured in series with the early DCT, thiazide diuretics promote renal K⁺ wasting by shifting Na⁺ reabsorption from early DCT to CNT; they promote alkalosis by shifting the remaining early DCT Na⁺ reabsorption to Na⁺/H⁺ exchange. This full DCT is suitable for simulating the defects of hyperkalemic hypertension, but the model offers no suggestion of a tight junction abnormality that might contribute to the phenotype.

sodium reabsorption; flow-dependent transport; collecting duct; thiazide diuretic

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