Active potassium absorption in rat distal colon.

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RESUMO

1. Active potassium (K+) absorption in rat distal colon was investigated by measuring mucosal-to-serosal (JK, ms) and serosal-to-mucosal (JK, sm) 42K+ fluxes (mu equiv h-1 cm-2) across isolated stripped mucosa under short-circuit conditions in normal and dietary Na-depleted animals. As previously demonstrated, removal of Na+ from both mucosal and serosal solutions bathing the normal colon slightly increased net K+ absorption as a result of inhibition of JK, sm without affecting JK, ms, while in the Na-depleted group net K+ secretion (-0.54 +/- 0.11) was converted to a marked net K+ absorption (1.68 +/- 0.30, P less than 0.001). 2. In both groups of animals in Na(+)-free Ringer solution, JK, ms exhibited saturable and linear components, while JK, sm was a linear function of [K+]. Estimated affinity constants (mM) for saturable net K+ absorption were similar in normal (0.52 +/- 0.12) and Na-depleted (0.67 +/- 0.11) animals; however, there was a greater than 3-fold increase in the saturable flux (Jmax) from 0.54 +/- 0.04 in the normal colon to 1.78 +/- 0.08 mu equiv h-1 cm-2 in Na-depleted animals. 3. Mucosal orthovanadate (100 microM) inhibited JK, ms in both normal (control, 0.66 +/- 0.05 vs. orthovanadate, 0.36 +/- 0.03 mu equiv h-1 cm-2, P less than 0.001) and Na-depleted animals (control 1.20 +/- 0.13 vs. orthovanadate 0.77 +/- 0.07 mu equiv h-1 cm-2, P less than 0.01) without affecting JK, sm or the short-circuit current. In the Na-depleted group mucosal omeprazole or SCH28080 (100 microM), inhibitors of gastric K(+)-H(+)-ATPase, insignificantly or slightly reduced (by 10%) JK, ms respectively; in contrast, mucosal ouabain (1 mM) markedly inhibited JK, ms (control, 1.61 +/- 0.16 vs. ouabain, 0.83 +/- 0.98 mu equiv h-1 cm-2, P less than 0.001). 4. Mucosal Na+ appeared to be a competitor of K+ uptake across the apical membrane. 5. These results indicate that dietary Na-depletion increases electroneutral K+ absorption by increasing its transport capacity and suggest that the mechanism of this active K+ absorption process may involve an apical K(+)-ATPase with properties that are unlike the gastric K(+)-H(+)-ATPase but similar, in part, to Na(+)-K(+)-ATPase.

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