1997年6月
Nitric oxide synthase and contractile protein in the rat cochlear lateral wall: Possible role of nitric oxide in regulation of strial blood flow
HEARING RESEARCH
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- 巻
- 108
- 号
- 1-2
- 開始ページ
- 65
- 終了ページ
- 73
- 記述言語
- 英語
- 掲載種別
- DOI
- 10.1016/S0378-5955(97)00041-5
- 出版者・発行元
- ELSEVIER SCIENCE BV
The present study demonstrated by histochemical and immunohistochemical methods that NADPH diaphorase reactivity, endothelial nitric oxide synthase (eNOS)-like immunoreactivity, and tropomyosin-like immunoreactivity, were located within the rat cochlear lateral wall. Both NADPH diaphorase reactivity and eNOS-like immunoreactivity were found mainly in the endothelium of the strial capillaries (ESC) and that of the vessels of the spiral ligament (ESL). These reaction products appeared to be somewhat more common in the ESC than in the ESL. On the other hand, tropomyosin-like immunoreactivity was localized in tissues outside the endothelium and its intensity was greater in the ESL than in the ESC. These findings suggest that nitric oxide (NO) produced by eNOS may play a role in regulating the blood flow of the cochlear lateral wall. In addition, NADPH diaphorase reactivity, eNOS-like immunoreactivity, and tropomyosin-like immunoreactivity showed different patterns of distribution between ESC and ESL. This suggests that in these two sites blood circulation is controlled by NO through two different mechanisms that are suitable for regulating strial blood flow.
Web of Science ® 被引用回数 : 30
Web of Science ® の 関連論文(Related Records®)ビュー
- リンク情報
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- DOI
- https://doi.org/10.1016/S0378-5955(97)00041-5
- CiNii Articles
- http://ci.nii.ac.jp/naid/10017042818
- PubMed
- https://www.ncbi.nlm.nih.gov/pubmed/9213123
- Web of Science
- https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:A1997XG68900008&DestApp=WOS_CPL
- ID情報
-
- DOI : 10.1016/S0378-5955(97)00041-5
- ISSN : 0378-5955
- CiNii Articles ID : 10017042818
- PubMed ID : 9213123
- Web of Science ID : WOS:A1997XG68900008