Chapter 8 Cell Models of Potassium Transport in the Renal Tubule

Abstract

Publisher Summary This chapter discusses the four modes of potassium (K) transport that have been identified in tubule cells: (1) the active ATPase-dependent Na–K exchange pump in the basolateral cell membrane, (2) the passive leak conductance of K, (3) the cotransport system of sodium (Na), chloride and K, and (4) electroneutral K chloride cotransport. They are ultimately responsible both for variable transepithelial net K transport and for maintaining cell K at optimal levels. It is, however, the unique segregation of these transport mechanisms to the two limiting barriers, the apical and basolateral cell membranes, that allows the control and regulation of both cell K homeostasis and transepithelial K movement. Whether K is secreted or reabsorbed across the renal tubule depends critically upon the apical cell membrane. The low K permeability of the brush-border membrane of proximal tubule cells minimizes leakage of K ions into the lumen. The regulation of K transport is mediated by the activation of specific renal and extrarenal stimuli acting on both basolateral and apical K transport mechanisms. The effective interaction of transport events between the basolateral and apical cell membrane safeguards the constancy of cell K content and cell volume of tubule cells despite large fluctuations of net transport of K and Na ions.