Abstract
The polar nature of epithelial cells in general has long been recognized. Thus, in the early work of Koefoed-Johnsen and Ussing (1) transepithelial sodium transport was attributed to passive apical uptake followed by active extrusion across the basolateral cell membranes. Subsequent work with electrophysiologic techniques, purified membrane vesicles, and other approaches has fully confirmed this basic model. Much of the information on epithelial asymmetry derives from studies on the renal proximal tubule, as repeatedly reviewed (2).
Proximal tubular reabsorption and secretion, responsible for transporting large amounts of many solutes, are processes mediated by various asymmetric carrier systems. For instance, p-aminohippurate (PAH) is actively accumulated at the basolateral cell membranes, with a facilitated diffusion step responsible for its further transfer from epithelial cell into the lumen (3). Fractional reabsorption of amino acids is determined by the rate of active uptake at the apical cell membranes (4). Much less attention has been paid to the possible role of basolateral amino acid transport in reabsorption and in cellular nutrition. The present review will focus on the nature and the physiologic significance of basolateral amino acid transport in the proximal renal tubule.
Following the work of Cross and Taggart (5) on PAH accumulation in slices of the renal cortex, this convenient preparation became popular for studying the renal handling of sugars and amino acids. However, as pointed out by Foulkes (6), the length of the diffusion pathway through partially (or completely) collapsed tubular lumina makes it likely that a major fraction of accumulation in slices results from basolateral uptake, even though the possibility cannot be excluded that a solute could reach the apical membranes by leakage between cells, i.e., along paracellular pathways.
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