LOOP-DIURETIC INHIBITION OF ADRENALINE-STIMULATED Cl- SECRETION IN A CULTURED EPITHELIUM OF RENAL ORIGIN (MDCK)

¹ Department of Physiology and Pharmacology, University of St Andrews, St Andrews, Fife KY16 9TS
² Department of Physiological Sciences, University of Newcastle-upon-Tyne, The Medical School, Framlington Place, Newcastle-upon-Tyne NE2 4HH

Loop diuretics (furosemide, bumetanide, piretanide) inhibit the adrenaline-stimulated short-circuit current due to transepithelial Cl^- secretion in cultured renal epithelial layers (MDCK). The inhibition of Cl^- secretion by loop diuretics is consistent with the presence of basal-lateral ‘cotransport’ since inhibition is observed only with the basal applications of loop diuretics, is of high potency (half-maximal bumetanide inhibition being observed at 0·8 µM, bumetanide being more potent than furosemide) and is without effect upon the adrenaline-stimulated increase in tissue conductance. Loop diuretics are also shown to inhibit a component of K⁺ efflux across the basal-lateral surfaces. Cellular uptake of [³H]bumetanide across both apical and basal surfaces of intact epithelial layers was measured in order to localize the cotransport system. A component of cellular [3H]bumetanide uptake sensitive to competition by 0·1 mM unlabelled loop diuretic is only observed from the basal-lateral cell surfaces. There is no evidence for transepithelial bumetanide secretion as is seen in renal cortex.

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