Regulation of potassium conductance by prostaglandins in cultured renal epitheloid (Madin-Darby canine kidney) cells

Abstract

Madin-Darby canine kidney (MDCK) cells form arachidonic acid metabolites following stimulation of several hormones known to modify the ion conductances at the plasma membrane. The present study has been performed to elucidate the influence of arachidonic acid on the electrical properties of subconfluent MDCK cells. As a result, arachidonic acid (1 or 10 mumol/l) leads to a transient hyperpolarization of the cell membrane, followed by a transient depolarization and a second, sustained hyperpolarization. The effects are inhibited by cycloxygenase inhibitor indomethacin (1 mumol/l). The initial transient hyperpolarization is mimicked by prostaglandin E2 (PGE2, 0.1 mumol/l), the sustained hyperpolarization by both PGE2 (0.1 mumol/l) and PGF2 alpha (0.1 mumol/l). The transient hyperpolarization is paralleled by an increase of potassium selectivity and a decrease of cell membrane resistance and is thus the result of increased potassium conductance. The transient depolarization is paralleled by an increase of chloride selectivity, reflecting an increase of chloride conductance. The sustained hyperpolarization is paralleled by an increase of cell membrane resistance, and increase of potassium selectivity and a decrease of chloride selectivity, and is thus the result of decreasing chloride conductance. The observations reveal a role of prostaglandins in the regulation of ion conductances in MDCK cells, which could well participate in the transport regulation by hormones.