Active potassium transport by rabbit descending colon epithelium.

Previous studies of rabbit descending colon have disagreed concerning potassium transport across this epithelium. Some authors reported active K+ secretion under in vitro short-circuited conditions, while others suggested that K+ transport occurs by passive diffusion through a highly potassium-selective paracellular route. For this reason, we re-examined potassium fluxes across the colon in the presence of specific and general metabolic inhibitors. In addition, electrochemical driving forces for potassium across the apical and basolateral membranes were measured using conventional and ion-sensitive microelectrodes. Under normal conditions a significant net K+ secretion was observed (JK net = -0.39 +/- 0.081 mueq/cm2hr) with 42K fluxes, usually reaching steady-state within approximately 50 min following isotope addition. In colons treated with serosal addition of 10(-4)M ouabain, JKsm was lowered by nearly 70% and JKms was elevated by approximately 50%. Thus a small but significant net absorption was present (JKnet = 0.12 +/- 0.027 mueq/cm2hr). Under control conditions, the net cellular electrochemical driving force for K+ was 17mV, favoring K+ exit from the cell. Cell potential measurements indicated that potassium remained above equilibrium after ouabain, assuming that passive membrane permeabilities are not altered by this drug. Net K+ fluxes were abolished by low temperature. The results indicate that potassium transport by the colon may occur via transcellular mechanisms and is not solely restricted to a paracellular pathway. These findings are consistent with our previous electrical results which indicated a nonselective paracellular pathway. Thus potassium transport across the colon can be modeled as a paracellular shunt pathway in parallel with pump-leak systems on the apical and basolateral membranes.