Energy-dependent transport of digoxin across renal tubular cell monolayers (LLC-PK1)

S. Ito, G. Koren, P. A. Harper, M. Silverman

Research output: Contribution to journalArticlepeer-review

38 Scopus citations


Digoxin secretory transport across renal tubular cell monolayers (LLC-PK1) grown on permeable filters was characterized. Metabolic inhibitors reduced total and specific basolateral to apical (B-A) flux of digoxin and conversely increased the apical to basolateral (A-B) flux. The specific transport of digoxin from the basolateral to the apical compartment was saturable, with a maximum velocity of transport of 184.5 ± 38.0 pmol · cm-2 · h-1 and a Michaelis-Menten constant (K(m)) of 14.1 ± 1.6 μM. In addition, B-A flux of digoxin resulted in accumulation of digoxin in the apical compartment against the concentration gradient. P-Glycoprotein inhibitors such as quinidine, verapamil, vincristine, and cyclosporine increased the net A-B flux and inhibited the total B-A flux without affecting the nonspecific flux significantly. Tetraethylammonium, a prototype substrate for an organic cation transport system, had no such effect. Our results suggest that digoxin undergoes transepithelial secretion by an energy-dependent, carrier-mediated process in renal tubules, a process that seems to be distinct from the tetraethylammonium transport system.

Original languageEnglish
Pages (from-to)40-47
Number of pages8
JournalCanadian Journal of Physiology and Pharmacology
Issue number1
StatePublished - 1993
Externally publishedYes


  • P-glycoprotein
  • cyclosporin e
  • quinidine
  • renal tubular secretion of digoxin
  • tetraethylammonium
  • verapamil
  • vincristine


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