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- 平田 結喜緒
- 東京医科歯科大学第2内科
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説明
Nitric oxide (NO) is a gas radical generated from 1-arginine via enzymatic action of NO synthases (NOS) in the presence of calmodulin (CaM), NADPH, flavins (FMN, FAD), tetrahydrobiopterine, O2, and heme. NOS contains reductase domain at C-terminus and oxygenase domain at N-terminus. At least three isoforms of NOS exist. Neuronal and endothelial constitutive (c) NOS is a Ca2+/CaM dependent, while inducible (i) NOS is Ca2+ independent. NO generated by neuronal cNOS functions as a neurotransmitter in the central as well as in the peripheral neurons, while NO by endothelial cNOS regulates vascular tonus. iNOS is regulated at the transcriptional level by several cytokines and endotoxins. Overproduction of NO by iNOS in a variety of cells, such as macrophages, vascular endothelial and smooth muscle cells, cardiocytes etc., functions as a host defence mechanism by its bacteriocidal action. However, sustained and exaggerated production of NO contributes to the development of endotoxin shock and organ dysfunction associated with sepsis, and many localized inflammatory lesions. Regulation of three NOS isoforms genes, their knock-out gene mice, and their structure·function are reviewed.
収録刊行物
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- Folia Endocrinologica Japonica
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Folia Endocrinologica Japonica 73 (1), 1-9, 1997
The Japan Endocrine Society
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詳細情報 詳細情報について
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- CRID
- 1390282681411559808
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- NII論文ID
- 10006806706
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- NII書誌ID
- AN00195891
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- COI
- 1:CAS:528:DyaK2sXitFyjtrg%3D
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- ISSN
- 00290661
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- 本文言語コード
- ja
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- データソース種別
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- JaLC
- Crossref
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可