Cell swelling increases a barium-inhibitable potassium conductance in the basolateral membrane of Necturus small intestine.

Abstract

Previous studies have shown that, immediately after the addition of galactose or alanine to the solution bathing the mucosal surface of Necturus small intestine, there is a rapid depolarization of the electrical potential difference across the mucosal membrane (.psi.mc). This is followed by a repolarization of .psi.mc that is paralleled by an increase in the ratio of the effective resistance of the mucosal membrane to that of the basolateral membrane (rm/rs); the latter was shown to be, at least in part, due to a marked increase in the conductance of the basolateral membrane. The following is reported. Exposure of this epithelium to a 12% hypotonic solution results in a hyperpolarization of .psi.mc and an increase in rm/rs. These effects are blocked by metabolic inhibitors and by the presence of 5 mM Ba2+ in the bathing solution; indeed, in the presence of Ba2+, .psi.mc depolarizes and rm/rs decreases to low values. Addition of 15 mM galactose to the mucosal solution when the serosal solution alone contains 5 mM Ba2+ results in a depolarization of .psi. but no subsequent repolarization of .psi.mc or increase in rm/rs; however, .psi.mc repolarizes and rm/rs increases when Ba2+ is subsequently removed from the serosal bathing solution. The basolateral membrane normally possesses a Ba2+-inhibitable K conductance, which appears to be reduced in the presence of metabolic inhibitors. After exposure of the tissue to a hypotonic solution or the addition of galactose to the mucosal solution, this conductance increases. These responses can be blocked by metabolic inhibitors. The delayed response of this tissue to the addition of sugars or amino acids to the mucosal solution may be the result of cell swelling resulting from the intracellular accumulation of these solutes in osmotically active forms.