Effect of SNI-2011 on amylase secretion from parotid tissue in rats and in neuronal nitric oxide synthase knockout mice

Autor: Noriko Inoue, Hirokazu Iida, Zhenfang Yuan, Hajime Ishida, Yasuko Ishikawa
Rok vydání: 2003
Předmět:
Male
Benzylamines
Quinuclidines
Indoles
Phosphodiesterase Inhibitors
Nitric Oxide Synthase Type I
Benzoates
Mice
Parotid Gland
Amylase
Enzyme Inhibitors
Estrenes
Egtazic Acid
Chelating Agents
Mice
Knockout
Oxadiazoles
Sulfonamides
Penicillamine
Imidazoles
Pilocarpine
Azepines
Calcium Channel Blockers
Pyrrolidinones
NG-Nitroarginine Methyl Ester
Amylases
Signal transduction
Myosin light-chain kinase
Genotype
Carbazoles
Thiophenes
Biology
In Vitro Techniques
Muscarinic Agonists
Exocytosis
Alkaloids
Ca2+/calmodulin-dependent protein kinase
Gallic Acid
Quinoxalines
Cyclic GMP-Dependent Protein Kinases
Animals
Secretion
Nitric Oxide Donors
Pyrroles
Rats
Wistar
Protein kinase A
Myosin-Light-Chain Kinase
Protein Kinase Inhibitors
Secretory pathway
Pharmacology
Dose-Response Relationship
Drug
Molecular biology
Rats
Enzyme Activation
Guanylate Cyclase
Molsidomine
Type C Phospholipases
Calcium-Calmodulin-Dependent Protein Kinases
biology.protein
Calcium
Carbachol
Nitric Oxide Synthase
Calcium-Calmodulin-Dependent Protein Kinase Type 2
Zdroj: European journal of pharmacology. 464(2-3)
ISSN: 0014-2999
Popis: The effect of (+/-)cis-2-methylspilo(1,3-oxathiolane-5,3')quinuclidine (SNI-2011) on the secretory pathway of amylase in parotid tissues was investigated. SNI-2011-induced exocytosis was inhibited by a cell-permeable Ca(2+) chelator or inhibitors of calmodulin kinase II, neuronal nitric oxide synthase (nNOS), soluble guanyl cyclase, cyclic GMP-dependent protein kinase (PKG), and myosin light chain kinase, suggesting that these enzymes were coupled with the exocytosis. Stimulation with SNI-2011 of isolated rat parotid acinar cells loaded with 4,5-diaminofluorescein/diacetate (DAF-2/DA) induced a fast increase in DAF fluorescence corresponding to an increase in the NO production. SNI-2011-induced amylase secretion from parotid tissues in nNOS knockout mice has not been observed yet in spite of the expression of muscarinic M(3) receptors and the maintenance of secretory response to isoproterenol in the tissues. These results indicate the implication of the activation of Ca(2+)- and calmodulin-dependent enzymes and NOS-PKG signaling pathway in SNI-2011-induced amylase secretion from parotid acinar cells.
Databáze: OpenAIRE
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