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Dadun > Depósito Académico > CIMA (Centro de Investigación Médica Aplicada) > Área de Terapia génica y Hepatología > Genética molecular > DA - CIMA - Terapia génica y Hepatología - Genética molecular - Artículos de Revista >

Bicarbonate-rich choleresis induced by secretin in normal rat is taurocholate-dependent and involves AE2 anion exchanger
Autor(es) : Banales, J.M. (Jesús M.)
Arenas, F. (Fabián)
Rodriguez-Ortigosa, C.M. (Carlos M.)
Saez, E. (Elena)
Uriarte, I. (Iker)
Doctor, R.B. (R. Brian)
Prieto, J. (Jesús)
Medina, J.F. (Juan Francisco)
Palabras clave : Anion Transport Proteins/physiology
Antiporters/physiology
Bicarbonates/metabolism
Bile/secretion
Bile Ducts/drug effects
Secretin/pharmacology
Taurocholic Acid/physiology
Fecha incorporación: 2006
Editorial : Wiley Blackwell
Versión del editor: http://bit.ly/sLVXc7
ISSN: 1527-3350
Cita: Banales JM, Arenas F, Rodriguez-Ortigosa CM, Saez E, Uriarte I, Doctor RB, et al. Bicarbonate-rich choleresis induced by secretin in normal rat is taurocholate-dependent and involves AE2 anion exchanger. Hepatology 2006 Feb;43(2):266-275.
Resumen
Canalicular bile is modified along bile ducts through reabsorptive and secretory processes regulated by nerves, bile salts, and hormones such as secretin. Secretin stimulates ductular cystic fibrosis transmembrane conductance regulator (CFTR)-dependent Cl- efflux and subsequent biliary HCO3- secretion, possibly via Cl-/HCO3- anion exchange (AE). However, the contribution of secretin to bile regulation in the normal rat, the significance of choleretic bile salts in secretin effects, and the role of Cl-/HCO3- exchange in secretin-stimulated HCO3- secretion all remain unclear. Here, secretin was administered to normal rats with maintained bile acid pool via continuous taurocholate infusion. Bile flow and biliary HCO3- and Cl- excretion were monitored following intrabiliary retrograde fluxes of saline solutions with and without the Cl- channel inhibitor 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB) or the Cl-/HCO3- exchange inhibitor 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS). Secretin increased bile flow and biliary excretion of HCO3- and Cl-. Interestingly, secretin effects were not observed in the absence of taurocholate. Whereas secretin effects were all blocked by intrabiliary NPPB, DIDS only inhibited secretin-induced increases in bile flow and HCO3- excretion but not the increased Cl- excretion, revealing a role of biliary Cl-/HCO3- exchange in secretin-induced, bicarbonate-rich choleresis in normal rats. Finally, small hairpin RNA adenoviral constructs were used to demonstrate the involvement of the Na+-independent anion exchanger 2 (AE2) through gene silencing in normal rat cholangiocytes. AE2 gene silencing caused a marked inhibition of unstimulated and secretin-stimulated Cl-/HCO3- exchange. In conclusion, maintenance of the bile acid pool is crucial for secretin to induce bicarbonate-rich choleresis in the normal rat and that this occurs via a chloride-bicarbonate exchange process consistent with AE2 function.
Enlace permanente: http://hdl.handle.net/10171/20250
Aparece en las colecciones: DA - CIMA - Servicios de apoyo - Instalación radioactiva - Artículos
DA - CIMA - Terapia génica y Hepatología - Hepatología experimental - Artículos de revista
DA - CIMA - Terapia génica y Hepatología - Genética molecular - Artículos de Revista

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