Occurrence of passive furosemide-sensitive transmembrane potassium transport in cultured cells |
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Authors: | J.F. Aiton A.R. Chipperfield J.F. Lamb P. Ogden N.L. Simmons |
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Affiliation: | 1. Department of Physiology, University of St Andrews, St Andrews, KY16 9TS Fife U.K.;2. Department of Physiology, The University, Dundee DDl 4HN U.K. |
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Abstract: | Furosemide () inhibits a proportion of the total passive (ouabain-insensitive) K+ influx into primary chick heart cell cultures (85%), BC3H1 cells (75%), MDCK cells (40%) and HeLa cells (57%). This action of furosemide upon K+ influx is independent of ( inhibition since the furosemide-sensitive component of the K+ influx is identical in the presence and absence of ouabain (). For HeLa cells the passive, furosemide-sensitive component of K+ influx is markedly dependent upon the external K+, Na+ and Cl? content. Acetate, iodide and nitrate are ineffective as substitutes for Cl?, whereas Br? is partially effective. Partial Cl? replacement by NO3? gave an apparent affinity of 100 mM [Cl]. Na+ replacement by choline+ abolishes the furosemide-sensitive component, whereas Li+ replacement reduces this component by 48%. Partial Na+ replacement by choline+ gives an apparent affinity of 25 mM [Na+]. Variation in the external K+ content gives an affinity for the furosemide-sensitive component of approx. 1.0 mM. Furosemide inhibition of the passive K+ inflúx is of high affinity, half-maximal inhibition being observed at furosemide. Piretanide () and phloretin () inhibit the same component of passive K+ influx as furosemide; ethacrynic acid and amiloride () partially so. The stilbene, SITS (), was ineffective as an inhibitor of the furosemide-sensitive component. |
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Keywords: | Furosemide Ion flux Cotranport (Cultured cell) |
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