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Abstract

Using microperfusion techniques the following transport parameters of the proximal tubule were measured: 1. Isotonic fluid (Na⁺) absorption (J_Na). 2. Zero net flux concentration (electrochemical potential) differences which are proportional to the respective active transport rates of H⁺ Cglycodiazine), D-glucose (α-methyl-D-glycoside), L-histidine, inorganic phosphate and calcium ions. 3. Transtubular and transcellular electrical potential differences and transcellular resistances.
The following was found:
1. Ouabain (1mM) applied peritubularly in golden hamsters inhibited J_Na incompletely and the sodium-coupled (secondary active) transport processes of glucose, histidine, phosphate and Ca⁺⁺ by more than 80%. The H⁺ (glycodiazine) transport was not affected. Ouabain (1mM) plus acetazolamide (0.2 mM) inhibited J_Na completely.
2. In the rat, pCMB (0.2 mM) when applied long enough, inhibits J_Na completely. At a time of pCMB application when J_Na is reduced to 1/3, this substance inhibits the active H⁺ (glycodiazine) transport which must be considered to be a direct action of pCMB. Furthermore it inhibits the secondary active phosphate transport either directly or via the inhibition of Na⁺ and/or H⁺ transport. The secondary active glucose, histidine and Ca⁺⁺ transport are little affected by pCMB. pCMB reduces the cell potential, reversibly, yet leaves unchanged the resistance ratio of the luminal to peritubular cell membrane .
3. In the rat SITS inhibits J_Na moderately but the active H⁺ (glycodiazine) transport strongly. It does not affect the glucose transport.
On the basis of these and other results a hypothesis of the interaction of Na⁺ and H⁺ (HCO₃^-) transport is given.