Steidl M, Ritter M, Lang F
Institute for Physiology, University of Innsbruck, Austria.
Pflugers Arch. 1991 Jun;418(5):431-6. doi: 10.1007/BF00497769.
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.
犬肾上皮细胞（MDCK）在受到几种已知可改变质膜离子电导的激素刺激后会形成花生四烯酸代谢产物。本研究旨在阐明花生四烯酸对亚汇合MDCK细胞电特性的影响。结果显示，花生四烯酸（1或10μmol/L）会导致细胞膜短暂超极化，随后是短暂去极化和第二次持续性超极化。这些效应被环氧化酶抑制剂吲哚美辛（1μmol/L）抑制。最初的短暂超极化可被前列腺素E2（PGE2，0.1μmol/L）模拟，持续性超极化可被PGE2（0.1μmol/L）和前列腺素F2α（PGF2α，0.1μmol/L）模拟。短暂超极化伴随着钾选择性增加和细胞膜电阻降低，因此是钾电导增加的结果。短暂去极化伴随着氯选择性增加，反映了氯电导增加。持续性超极化伴随着细胞膜电阻增加、钾选择性增加和氯选择性降低，因此是氯电导降低的结果。这些观察结果揭示了前列腺素在MDCK细胞离子电导调节中的作用，这很可能参与了激素对转运的调节。
