Nonadrenergic, Noncholinergic Relaxation in Longitudinal Muscle of Rat Jejunum.
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- Niioka Satomi
- Department of Veterinary Pharmacology, College of Agriculture, Research Institute for Advanced Science and Technology, Osaka Prefecture University
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- Takeuchi Tadayoshi
- Department of Veterinary Pharmacology, College of Agriculture, Research Institute for Advanced Science and Technology, Osaka Prefecture University Department of Molecular Physiology and Biochemistry, Research Institute for Advanced Science and Technology, Osaka Prefecture University
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- Kishi Masami
- Department of Veterinary Pharmacology, College of Agriculture, Research Institute for Advanced Science and Technology, Osaka Prefecture University
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- Ishii Toshiaki
- Department of Veterinary Pharmacology, College of Agriculture, Research Institute for Advanced Science and Technology, Osaka Prefecture University Department of Molecular Physiology and Biochemistry, Research Institute for Advanced Science and Technology, Osaka Prefecture University
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- Nishio Hideaki
- Department of Veterinary Pharmacology, College of Agriculture, Research Institute for Advanced Science and Technology, Osaka Prefecture University
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- Takewaki Tadashi
- United Graduate School of Veterinary Sciences, Gifu University
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- Hata Fumiaki
- Department of Veterinary Pharmacology, College of Agriculture, Research Institute for Advanced Science and Technology, Osaka Prefecture University Department of Molecular Physiology and Biochemistry, Research Institute for Advanced Science and Technology, Osaka Prefecture University
書誌事項
- タイトル別名
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- Nonadrenergic Noncholinergic Relaxation
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抄録
The mediators of nonadrenergic, noncholinergic (NANC)relaxation in the longitudinal muscle of rat jejunum were studied in vitro. Electrical field stimulation (EFS)of segments of rat jejunum induced a rapid transient relaxation followed by a subsequent contraction in the presence of atropine and guanethidine. NG-Nitro-L-arginine (L-NOARG, 10 μM)inhibited the EFS-induced NANC relaxation by about 25%, and L-arginine (1 mM)completely reversed this inhibition. Exogenously added nitric oxide (0.1-10 μM)induced relaxation of the segment. Treatment of the segment with a-chymotrypsin resulted in about 50% inhibition of the EFS-induced relaxation. Several peptide candidates for the mediator of NANC relaxation were examined by using selective antagonists of their receptors or by a receptor-desensitization method. Results indicated that vasoactive intestinal peptide, pituitary adenylate cyclase activating peptide, peptide histidine isoleucine, atrial natriuretic peptide and neurotensin are not associated with NANC relaxation of the segments. On the other hand, apamin at 1 μM inhibited the EFS-induced relaxation by 74%. Inhibitory effects of L-NOARG and, apamin or α-chymotrypsin treatment on the EFS-induced relaxation were additive and almost complete. Exogenous nitric oxide-induced relaxation was not affected by apamin. Inhibitory junction potentials (i.j.p.''s)were recorded from longitudinal muscle cells of rat jejunum. Apamin at 200 nM abolished i.j.p.''s induced by two pulses of EFS. These results suggest that NANC relaxation in longitudinal muscle of rat jejunum involves two independent components: one is a nitric oxide-mediated minor component, and the other is an unknown substance-mediated apamin-sensitve major component that is inhibited by α-chymotrypsin treatment.
収録刊行物
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- Jpn.J.Pharmacol.
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Jpn.J.Pharmacol. 73 (2), 155-161, 1997
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390001204286959872
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- NII論文ID
- 10008677187
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- NII書誌ID
- AA00691188
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- COI
- 1:STN:280:ByiB38fpt1c%3D
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- ISSN
- 13473506
- 00215198
- http://id.crossref.org/issn/00215198
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- NDL書誌ID
- 4153690
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- PubMed
- 9074949
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可