P-glycoprotein-mediated renal tubular secretion of digoxin: the toxicological significance of the urine-blood barrier model
S Ito, C Woodland, PA Harper, G Koren - Life sciences, 1993 - Elsevier
S Ito, C Woodland, PA Harper, G Koren
Life sciences, 1993•ElsevierWe provide direct evidence that verapamil inhibits active digoxin secretion in renal tubular
cells (LLC-PK1), and that verapamil increases cellular accumulation of digoxin. These
findings suggest that verapamil inhibits the digoxin active secretory transport at the apical
membranes, supporting the theory that P-glycoprotein mediates digoxin secretion in the
renal tubular cells. Based on existing data on digoxin transport, we present a hypothetical
model for the renal handling of digoxin, implying that P-glycoprotein functions as a driving …
cells (LLC-PK1), and that verapamil increases cellular accumulation of digoxin. These
findings suggest that verapamil inhibits the digoxin active secretory transport at the apical
membranes, supporting the theory that P-glycoprotein mediates digoxin secretion in the
renal tubular cells. Based on existing data on digoxin transport, we present a hypothetical
model for the renal handling of digoxin, implying that P-glycoprotein functions as a driving …
Abstract
We provide direct evidence that verapamil inhibits active digoxin secretion in renal tubular cells (LLC-PK1), and that verapamil increases cellular accumulation of digoxin. These findings suggest that verapamil inhibits the digoxin active secretory transport at the apical membranes, supporting the theory that P-glycoprotein mediates digoxin secretion in the renal tubular cells. Based on existing data on digoxin transport, we present a hypothetical model for the renal handling of digoxin, implying that P-glycoprotein functions as a driving mechanism of a unidirectional “urine-blood” barrier.
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