Abstract
The involvement of particular intracellular signalling pathways in agonist-evoked degranulation of guinea pig pancreatic duct goblet cells was investigated. Carbachol, vasoactive intestinal peptide (VIP), calcium ionophore A23187, phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA), cyclic AMP analogue Sp-5,6-DCl-cBIMPS and forskolin each caused degranulation of goblet cells in isolated ducts. Degranulation induced by carbachol was not inhibited by okadaic acid, cytochalasin-D or nocodazole. These results indicate that at least two major signalling pathways are involved in pancreatic duct goblet cell secretion.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Calcimycin / pharmacology
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Carbachol / pharmacology
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Cell Degranulation*
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Colforsin / pharmacology
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Cyclic AMP-Dependent Protein Kinases / metabolism
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Cytochalasin D / pharmacology
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Dichlororibofuranosylbenzimidazole / analogs & derivatives
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Dichlororibofuranosylbenzimidazole / pharmacology
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Enzyme Activation
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Ethers, Cyclic / pharmacology
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Guinea Pigs
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In Vitro Techniques
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Male
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Nocodazole / pharmacology
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Okadaic Acid
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Pancreatic Ducts / cytology
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Pancreatic Ducts / drug effects
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Pancreatic Ducts / physiology*
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Protein Kinase C / metabolism
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Tetradecanoylphorbol Acetate / pharmacology
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Thionucleotides / pharmacology
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Vasoactive Intestinal Peptide / pharmacology
Substances
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Ethers, Cyclic
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Thionucleotides
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5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole-3',5'-monophosphorothioate
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Colforsin
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Okadaic Acid
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Cytochalasin D
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Vasoactive Intestinal Peptide
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Calcimycin
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Dichlororibofuranosylbenzimidazole
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Carbachol
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Cyclic AMP-Dependent Protein Kinases
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Protein Kinase C
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Tetradecanoylphorbol Acetate
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Nocodazole