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LOOP‐DIURETIC INHIBITION OF ADRENALINE‐STIMULATED Cl‐ SECRETION IN A CULTURED EPITHELIUM OF RENAL ORIGIN (MDCK)
Author(s) -
Brown C. D. A.,
Rugg E. L.,
Simmons N. L.
Publication year - 1986
Publication title -
quarterly journal of experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0144-8757
DOI - 10.1113/expphysiol.1986.sp002977
Subject(s) - bumetanide , cotransporter , furosemide , endocrinology , loop of henle , diuretic , medicine , chemistry , loop diuretic , basal (medicine) , secretion , bullfrog , nephron , kidney , biology , sodium , organic chemistry , insulin
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 [ 3 H]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.