Abstract

The present work explores the contributions of basolateral carrier systems in tubular reabsorption of organic solutes. Reabsorption of sugars and amino acids, as previously shown, can be represented by a three-compartment linear model that predicts that 1) if basolateral transport contributes to sugar reabsorption, alpha-methylglucoside reabsorption compared with that of glucose should be characterized by a longer transepithelial transit time (TET) and a correspondingly increased cellular transport pool (S), and 2) saturation of basolateral amino acid carriers, or presence of competing amino acids or other basolateral transport inhibitors, should prolong TET of a test amino acid, and increase S above the expected value. Both predictions were fully confirmed. Heavy metal intoxication not only inhibits transport of amino acids at the brush border, but also prolongs their TET and increases the size of S for a given reabsorbed load. Basolateral extrusion of amino acids is more sensitive to metals than is uptake across the brush border. Although basolateral carriers accelerate return of reabsorbed solute to blood, their contribution to reabsorption does not seem to be mandatory.

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