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Am J Physiol Gastrointest Liver Physiol (December 27, 2002). doi:10.1152/ajpgi.00302.2002
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Submitted on July 25, 2002
Accepted on December 16, 2002

Dopaminergic inhibition of secretin-stimulated choleresis by increased PKC-{gamma} expression and decrease of PKA activity

Shannon Glaser1, Domenico Alvaro2, Tania Roskams3, Jo Lynne Phinizy1, George Stoica4, Heather Francis1, Yoshiyuki Ueno5, Barbara Barbaro6, Marco Marzioni6, Jeremy Mauldin6, Sobia Rashid6, Maria Grazia Mancino2, Gene LeSage7, and Gianfranco Alpini8*

1 Division of Research and Education, Scott and White Hospital, Temple, TX, USA
2 Division of Gastroenterology, University of Rome, Rome, Italy
3 Department of Morphology and Molecular Pathology, University of Leuven, Leuven, Belgium
4 Texas A&M University, College Station, TX, USA
5 Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan
6 Department of Medical Physiology, The Texas A&M University System Health Science Center, Temple, TX, USA
7 Department of Internal Medicine, Scott and White Hospital, Temple, TX, USA
8 Department of Internal Medicine, Scott and White Hospital, Temple, TX, USA; Department of Medical Physiology, The Texas A&M University System Health Science Center, Temple, TX, USA; Department of Research, Central Texas Veterans Health Care System, Temple, TX, USA

* To whom correspondence should be addressed. E-mail: galpini{at}tamu.edu.

To determine the role and mechanisms of action by which dopaminergic innervation modulates ductal secretion in bile duct ligated (BDL) rats. Methods: We determined the expression of D1, D2 and D3 dopaminergic receptors in cholangiocytes. We evaluated whether D1, D2 (quinelorane) or D3 dopaminergic receptor agonists influence basal and secretin-stimulated choleresis, and lumen expansion in intrahepatic bile duct units (IBDU) and cAMP levels in cholangiocytes in the absence or presence of BAPTA/AM, chelerythrine, H7, or rottlerin. We evaluated if: (i) quinelorane effects on ductal secretion were associated with increased expression of Ca2+-dependent PKC isoforms; and (ii) increased expression of PKC causes inhibition of PKA activity. Results: Quinelorane inhibited secretin-stimulated choleresis in vivo, and IBDU lumen space, cAMP levels and PKA activity in cholangiocytes. The inhibitory effects of quinelorane on secretin-stimulated ductal secretion and PKA activity were blocked by BAPTA/AM, chelerythrine and H7. Quinelorane effects on ductal secretion were associated with activation the Ca2+-dependent PKC-{gamma} but not other PKC isoforms. Conclusion: The dopaminergic nervous system counter-regulates secretin-stimulated ductal secretion in experimental cholestasis.




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