Abstract
For obvious reasons the Na+-dependence of sugar and amino acid transport was described much earlier for the intestine (5, 15, 19, 61, 62) than for the kidney. Thus, the Na+-sugar cotransport hypothesis was already well for mulated (15) before the sodium dependence of renal glucose transport had been reported in perfused rat (64) and frog kidney (91, 92) and in rabbit kidney cortex slices (52). Similarly, the sodium dependence of renal amino acid transport was studied by uptake into tubular cells (24, 40, 41, 69, 70, 71, 79) before the introduction of new techniques, such as the doubly perfused proximal tubule in situ (86), with transtubular or cellular electrical potential measurements (30) and the preparation of osmotically reactive plasma membrane vesicles from either cell side (51), made it possible to study the single transport steps and to test the sodium gradient hypothesis rigorously. The vesicular transport studies have already been reviewed extensively (48, 65).
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