Progesterone causes natriuresis, an effect largely attributed to displacement of aldosterone from its receptor. The present study, however, demonstrates that progesterone (0.1,1, and 10-mu-mol/1, also causes a rapid, fully reversible depolarization of Madin-Darby canine kidney (MDCK) cells (by 1.3 +/- 0.5, 4.1 +/- 0.7 and 12.3 +/- 1.5 mV, respectively). 17-alpha-Hydroxyprogesterone and dihydroxytestosterone are, by two orders of magnitude, less effective, whereas cholesterol, aldosterone, hydrocortisone, and estradiol (each up to 10-mu-mol/l) did not significantly alter the potential difference across the cell membrane. The effect of progesterone is blunted by antiprogestogen RU 486 (5-mu-mol/l). The progesterone-induced depolarization is paralleled by a decrease of potassium selectivity and an increase of cell membrane resistance and is abolished in the presence of the potassium channel blocker barium (10 mmol/l), as well as in the presence of 40 mmol/l potassium in the extracellular fluid. Neither removal of extracellular chloride or bicarbonate nor amiloride, ouabain, or pretreatment with pertussis toxin abolish the depolarizing effect of 5-mu-mol/l progesterone. In conclusion, acute administration of progesterone depolarizes MDCK cells by decreasing the potassium conductance of the cell membrane.
Useful keywords (using NLM MeSH Indexing)
Dose-Response Relationship, Drug
Membrane Potentials/drug effects
Potassium Channels/drug effects
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