Abstract
Treatment of rat 3Y1 fibroblasts with vasopressin (AVP) results in a transient activation of MAP kinase as potent as with EGF and serum. An antagonist of vasopressin receptor V1, but not an antagonist of V2, inhibited the AVP-induced activation of MAP kinases, indicating that AVP activates MAP kinases through V1 receptor. Prolonged TPA treatment of cells resulted in partial MAP kinase activation, indicating the presence of PKC-independent pathway. The pathway was inhibited by wortmannin, an inhibitor of PI3-kinase. The results suggest that wortmannin-sensitive molecules such as PI3-kinase, are involved in the V1 receptor-mediated activation of the MAP kinase pathway independent of TPA-sensitive PKC.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Androstadienes / pharmacology*
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Animals
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Antidiuretic Hormone Receptor Antagonists
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Arginine Vasopressin / pharmacology
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Benzazepines / pharmacology
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Calcium-Calmodulin-Dependent Protein Kinases / metabolism*
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Cells, Cultured
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Deamino Arginine Vasopressin / pharmacology
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Dose-Response Relationship, Drug
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Enzyme Activation / drug effects
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Enzyme Inhibitors / pharmacology*
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Fibroblasts / cytology
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Mitogen-Activated Protein Kinase 1
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Mitogen-Activated Protein Kinase 3
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Mitogen-Activated Protein Kinases*
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Piperidines / pharmacology
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Quinolones / pharmacology
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Rats
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Receptors, Vasopressin / agonists
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Receptors, Vasopressin / drug effects
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Receptors, Vasopressin / metabolism*
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Signal Transduction / drug effects*
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Tetradecanoylphorbol Acetate / pharmacology
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Wortmannin
Substances
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Androstadienes
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Antidiuretic Hormone Receptor Antagonists
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Benzazepines
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Enzyme Inhibitors
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Piperidines
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Quinolones
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Receptors, Vasopressin
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Arginine Vasopressin
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OPC 21268
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mozavaptan
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Calcium-Calmodulin-Dependent Protein Kinases
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Mitogen-Activated Protein Kinase 1
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Mitogen-Activated Protein Kinase 3
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Mitogen-Activated Protein Kinases
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Deamino Arginine Vasopressin
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Tetradecanoylphorbol Acetate
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Wortmannin