Nitrergic Inhibition of Tachykininergie Neuro-Muscular Transmission via Cyclic GMP in the Hamster Ileum
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- Matsuyama Hayato
- Laboratory of Veterinary Pharmacology, Department of Veterinary Medicine, Faculty of Applied Biological Science, Gifu University
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- UNNO Toshihiro
- Laboratory of Veterinary Pharmacology, Department of Veterinary Medicine, Faculty of Applied Biological Science, Gifu University
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- KOMORI Seiichi
- Laboratory of Veterinary Pharmacology, Department of Veterinary Medicine, Faculty of Applied Biological Science, Gifu University
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- Takewaki Tadashi
- Laboratory of Veterinary Physiology, Department of Veterinary Medicine, Faculty of Applied Biological Science, Gifu University
Bibliographic Information
- Other Title
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- Pharmacology: Nitrergic inhibition of tachykininergic neuro-muscular transmission via cyclic GMP in the hamster ileum
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Abstract
The present study was designed to explore the inhibitory mechanism by nitric oxide (NO) of the tachykininergic neuro-muscular transmissions in the hamster ileum. In the presence of guanethidine (1 μM), atropine (0.5 μM), nifedipine (0.1 μM) and apamin (100 nM), electrical field stimuli (EFS; 0.5 ms duration, 15 V) evoked non-adrenergic, non-cholinergic excitatory junction potentials (EJPs) in circular smooth muscle cells. The EJPs were markedly inhibited by the tachykinin NK1 receptor antagonists [D-Pro4, D-Trp7,9]-SP(4-11) (3 μM). Both the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 200 μM) and the soluble guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one (ODQ, 10 μM), did not affect on the resting membrane potentials, but enhanced the tachykininergic EJPs. In the presence of L-NAME (200 μM), exogenously applied NO (10 μM) and the membrane permeable analogue of guanosine 3',5'-cyclic monophosphate (cGMP), 8-bromoguanosine 3',5'-cyclic monophosphate (8-Br-cGMP, 3 mM), significantly inhibited the tachykininergic EJPs. Application of EFS (0.5 msec duration, 15 V) with trains of 20 pulses at 20 Hz increased amount of released substance P (SP). The release of SP was further increased by the treatment of L-NAME or ODQ, but markedly reduced by exogenously applied NO and 8-Br-cGMP. These results suggest that the endogenous NO may inhibit the tachykininergic neuro-muscular transmissions by the decrease of SP release from the tachykininergic neurons, possibly through a guanylate cyclase-cGMP-dependent mechanism in the hamster ileum.<br>
Journal
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- Journal of Veterinary Medical Science
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Journal of Veterinary Medical Science 73 (4), 453-458, 2011
JAPANESE SOCIETY OF VETERINARY SCIENCE
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Details 詳細情報について
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- CRID
- 1390282681407918720
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- NII Article ID
- 130000444585
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- NII Book ID
- AA10796138
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- ISSN
- 13477439
- 09167250
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- NDL BIB ID
- 11104748
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- Text Lang
- en
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- Data Source
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- JaLC
- NDL
- Crossref
- CiNii Articles
- KAKEN
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- Abstract License Flag
- Disallowed