Active potassium absorption in rat distal colon.

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.