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Vol. 57, Issue 1, 59-67, January 2000
Department of Pharmacology and Toxicology, University of Nijmegen,
Nijmegen, The Netherlands (R.M., S.A.T., R.A.M.H. van A., F.G.M.R.);
Laboratory of Pharmacology and Chemistry, NIEHS/National Institutes of
Health, Research Triangle Park, North Carolina (D.S.M.); and Mount
Desert Island Biological Laboratory, Salisbury Cove, Maine (R.M.,
S.A.T., D.S.M.)
In the kidney, endothelins (ETs) are important regulators of blood
flow, glomerular hemodynamics, and sodium and water homeostasis. They
have been implicated in the pathophysiology of acute ischemic renal
failure, nephrotoxicity by cyclosporine, cisplatin and radiocontrast agents, and vascular rejection of kidney transplants. Here, we used
intact killifish renal proximal tubules, fluorescent substrates for
Mrp2 (fluorescein-methotrexate, FL-MTX) and P-glycoprotein (a
fluorescent CSA derivative, NBD-CSA), and confocal microscopy to reveal
a new role for renal ET: regulation of ATP-driven drug transport in
proximal tubule. Subnanomolar to nanomolar concentrations of ET-1
rapidly reduced the cell-to-tubular lumen transport of both fluorescent
compounds. These effects were prevented by an ETB receptor
antagonist but not by an ETA receptor antagonist. Immunostaining with an antibody to mammalian ETB receptors
showed specific localization to the basolateral membrane of the fish tubular epithelial cells. ET-1 effects on transport were blocked by
protein kinase C-selective inhibitors, implicating protein kinase C in
ET-1 signaling. Finally, the nephrotoxic radiocontrast agent iohexol
reduced cell-to-lumen FL-MTX and NBD-CSA transport, and these effects
were abolished by an ETB receptor antagonist. These are the
first results linking ET to the control of xenobiotic transport and the
first demonstrating control of renal multidrug resistance-associated
protein 2 and P-glycoprotein by a hormone.
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