Influence of glucose absorption on ion activities in cells and submucosal space in goldfish intestine.

Mucosal glucose addition evokes in goldfish intestinal epithelium a fast depolarization of the mucosal membrane potential (delta psi mc = 12 mV) followed by a slower repolarization (delta psi mc = -7 mV). The intracellular sodium activity, aiNa+, rises from 13.2 +/- 2.4 meq/l by 6.7 +/- 0.5 meq/l within 5 min, aiCl- rises about 3 meq/l above the control value of 37.7 +/- 2.2 meq/l, while aiK is constant (97.7 +/- 7.4 meq/l). The potassium activity measured in the submucosal interstitium near the basal side of the cells (asK+) is 5.2 +/- 0.2 meq/l in non-absorbing tissue compared to 4.2 meq/l in the bathing solution and shows a transient increase due to glucose absorption (1.1 +/- 0.1 meq/l). In chloride-free media asK+ = 4.2 +/- 0.1 meq/l and psi mc hyperpolarizes by -13 mV. The depolarization due to glucose absorption increases (delta psi mc = 14.1 +/- 1.4) and the repolarization (delta psi repolmc) disappears. In addition, aiNa+ rises from 16.3 +/- 2.4 meq/l by 9.9 +/- 1.5 meq/l within 5 min, aiK+ remains constant and equal to the value in chloride containing solutions (88.5 +/- 2.8 meq/l); asK+ increases transiently (1.1 +/- 0.1 meq/l). Serosal Ba2+ (5 mM) depolarizes psi mc (+14.2 +/- 1.0 mV) and abolishes the repolarization. Increased serosal or mucosal potassium activity depolarizes psi mc and abolishes the repolarization. These effects are discussed in terms of changes of ion activities, the basolateral potassium conductance, the influence of intracellular Ca2+, the functional state of the Na/K-pump, and modulation of membrane permeabilities by extracellular potassium.