Tetraethylammonium block of water flux in Aquaporin-1 channels expressed in kidney thin limbs of Henle's loop and a kidney-derived cell line

Persistent Link:
http://hdl.handle.net/10150/610074
Title:
Tetraethylammonium block of water flux in Aquaporin-1 channels expressed in kidney thin limbs of Henle's loop and a kidney-derived cell line
Author:
Yool, Andrea; Brokl, Olga; Pannabecker, Thomas; Dantzler, William; Stamer, W. D.
Affiliation:
Dept of Physiology, University of Arizona College of Medicine, Tucson, Arizona, USA; Dept of Pharmacology, University of Arizona College of Medicine, Tucson, Arizona, USA; Dept of Opthalmology, University of Arizona College of Medicine, Tucson, Arizona, USA
Issue Date:
2002
Publisher:
BioMed Central
Citation:
BMC Physiology 2002, 2:4 http://www.biomedcentral.com/1472-6793/2/4
Journal:
BMC Physiology
Rights:
© 2002 Yool et al; licensee BioMed Central Ltd. Verbatim copying and redistribution of this article are permitted in any medium for any purpose, provided this notice is preserved along with the article's original URL.
Collection Information:
This item is part of the UA Faculty Publications collection. For more information this item or other items in the UA Campus Repository, contact the University of Arizona Libraries at repository@u.library.arizona.edu.
Abstract:
BACKGROUND:Aquaporin-1 (AQP1) channels are constitutively active water channels that allow rapid transmembrane osmotic water flux, and also serve as cyclic-GMP-gated ion channels. Tetraethylammonium chloride (TEA; 0.05 to 10 mM) was shown previously to inhibit the osmotic water permeability of human AQP1 channels expressed in Xenopus oocytes. The purpose of the present study was to determine if TEA blocks osmotic water flux of native AQP1 channels in kidney, and recombinant AQP1 channels expressed in a kidney derived MDCK cell line. We also demonstrate that TEA does not inhibit the cGMP-dependent ionic conductance of AQP1 expressed in oocytes, supporting the idea that water and ion fluxes involve pharmacologically distinct pathways in the AQP1 tetrameric complex.RESULTS:TEA blocked water permeability of AQP1 channels in kidney and kidney-derived cells, demonstrating this effect is not limited to the oocyte expression system. Equivalent inhibition is seen in MDCK cells with viral-mediated AQP1 expression, and in rat renal descending thin limbs of Henle's loops which abundantly express native AQP1, but not in ascending thin limbs which do not express AQP1. External TEA (10 mM) does not block the cGMP-dependent AQP1 ionic conductance, measured by two-electrode voltage clamp after pre-incubation of oocytes in 8Br-cGMP (10-50 mM) or during application of the nitric oxide donor, sodium nitroprusside (2-4 mM).CONCLUSIONS:TEA selectively inhibits osmotic water permeability through native and heterologously expressed AQP1 channels. The pathways for water and ions in AQP1 differ in pharmacological sensitivity to TEA, and are consistent with the idea of independent solute pathways within the channel structure. The results confirm the usefulness of TEA as a pharmacological tool for the analysis of AQP1 function.
EISSN:
1472-6793
DOI:
10.1186/1472-6793-2-4
Version:
Final published version
Additional Links:
http://www.biomedcentral.com/1472-6793/2/4

Full metadata record

DC FieldValue Language
dc.contributor.authorYool, Andreaen
dc.contributor.authorBrokl, Olgaen
dc.contributor.authorPannabecker, Thomasen
dc.contributor.authorDantzler, Williamen
dc.contributor.authorStamer, W. D.en
dc.date.accessioned2016-05-20T08:57:58Z-
dc.date.available2016-05-20T08:57:58Z-
dc.date.issued2002en
dc.identifier.citationBMC Physiology 2002, 2:4 http://www.biomedcentral.com/1472-6793/2/4en
dc.identifier.doi10.1186/1472-6793-2-4en
dc.identifier.urihttp://hdl.handle.net/10150/610074-
dc.description.abstractBACKGROUND:Aquaporin-1 (AQP1) channels are constitutively active water channels that allow rapid transmembrane osmotic water flux, and also serve as cyclic-GMP-gated ion channels. Tetraethylammonium chloride (TEAen
dc.description.abstract0.05 to 10 mM) was shown previously to inhibit the osmotic water permeability of human AQP1 channels expressed in Xenopus oocytes. The purpose of the present study was to determine if TEA blocks osmotic water flux of native AQP1 channels in kidney, and recombinant AQP1 channels expressed in a kidney derived MDCK cell line. We also demonstrate that TEA does not inhibit the cGMP-dependent ionic conductance of AQP1 expressed in oocytes, supporting the idea that water and ion fluxes involve pharmacologically distinct pathways in the AQP1 tetrameric complex.RESULTS:TEA blocked water permeability of AQP1 channels in kidney and kidney-derived cells, demonstrating this effect is not limited to the oocyte expression system. Equivalent inhibition is seen in MDCK cells with viral-mediated AQP1 expression, and in rat renal descending thin limbs of Henle's loops which abundantly express native AQP1, but not in ascending thin limbs which do not express AQP1. External TEA (10 mM) does not block the cGMP-dependent AQP1 ionic conductance, measured by two-electrode voltage clamp after pre-incubation of oocytes in 8Br-cGMP (10-50 mM) or during application of the nitric oxide donor, sodium nitroprusside (2-4 mM).CONCLUSIONS:TEA selectively inhibits osmotic water permeability through native and heterologously expressed AQP1 channels. The pathways for water and ions in AQP1 differ in pharmacological sensitivity to TEA, and are consistent with the idea of independent solute pathways within the channel structure. The results confirm the usefulness of TEA as a pharmacological tool for the analysis of AQP1 function.en
dc.language.isoenen
dc.publisherBioMed Centralen
dc.relation.urlhttp://www.biomedcentral.com/1472-6793/2/4en
dc.rights© 2002 Yool et al; licensee BioMed Central Ltd. Verbatim copying and redistribution of this article are permitted in any medium for any purpose, provided this notice is preserved along with the article's original URL.en
dc.titleTetraethylammonium block of water flux in Aquaporin-1 channels expressed in kidney thin limbs of Henle's loop and a kidney-derived cell lineen
dc.typeArticleen
dc.identifier.eissn1472-6793en
dc.contributor.departmentDept of Physiology, University of Arizona College of Medicine, Tucson, Arizona, USAen
dc.contributor.departmentDept of Pharmacology, University of Arizona College of Medicine, Tucson, Arizona, USAen
dc.contributor.departmentDept of Opthalmology, University of Arizona College of Medicine, Tucson, Arizona, USAen
dc.identifier.journalBMC Physiologyen
dc.description.collectioninformationThis item is part of the UA Faculty Publications collection. For more information this item or other items in the UA Campus Repository, contact the University of Arizona Libraries at repository@u.library.arizona.edu.en
dc.eprint.versionFinal published versionen
All Items in UA Campus Repository are protected by copyright, with all rights reserved, unless otherwise indicated.