Thrombin-Induced Responses Via Protease-Activated Receptor 1 Blocked by the Endothelium on Isolated Porcine Retinal Arterioles 11

• Material Type: 博士論文
• ISSN: 0271-3683
• Title: Thrombin-Induced Responses Via Protease-Activated Receptor 1 Blocked by the Endothelium on Isolated Porcine Retinal Arterioles
• Volume: 43 11
• Author/Editor: 髙橋, 賢伍
• Publication Date: 2018-11
• Publication Date (W3CDTF): 2018-11
• Periodical title: Current eye research
• Degree grantor/type: 旭川医科大学
• Date Granted: 2018-09-28
• Date Granted (W3CDTF): 2018-09-28
• Dissertation Number: 甲第526号
• Degree Type: 博士（医学）
• Conferring No. (Dissertation): 甲第526号
• Text Language Code: eng
• Subject Heading: PAR-1; Thrombin; endothelium blood retinal barrier; protease-activated receptor 1; vasoconstriction; vasorelaxation
• Note (General): PURPOSE: Thrombin, a serine protease, causes organ-specific responses to vessels. However, the mechanism by which thrombin affects the retinal microcirculation remains unclear. We examined the effects of thrombin on the retinal microvasculature and signaling mechanisms. METHODS: Porcine retinal arterioles were isolated, cannulated, and pressurized (55 cmH2O) without flow in this in vitro study. Videomicroscopy techniques recorded changes in diameter in the retinal arterioles in response to thrombin at concentrations ranging from 0.001 to 20 mU/ml. RESULTS: Extraluminal administration of thrombin induced concentration-dependent vascular responses, that is, vasoconstriction at low concentrations less than 5 mU/ml and vasorelaxation with high concentrations greater than 5 mU/ml. However, intraluminal administration of thrombin (5 mU/m) did not constrict the retinal arterioles; in denuded vessels, intraluminal administration constricted the retinal arterioles. Thrombin-induced vasoconstriction was significantly (p < 0.01) suppressed by pretreatment with a protein kinase C (PKC) inhibitor and a protease-activated receptor (PAR)-1 inhibitor but not by PAR-2 and PAR-4 inhibitors or denudation. A rho kinase (ROCK) inhibitor also suppressed thrombin-induced vasoconstriction (5 mU/ml) compared with sodium nitroprusside. Endothelial denudation and pretreatment with an endothelial nitric oxide (NO) synthase inhibitor suppressed vasorelaxation caused by a high concentration of thrombin. CONCLUSIONS: A low concentration of thrombin causes vasoconstriction of smooth muscles via PAR-1, PKC, and ROCK, and a high concentration of thrombin possibly causes vasorelaxation of the retinal arterioles via nitric oxide synthase activation in the endothelium. The vascular endothelium might block signaling of thrombin-induced vasoconstriction in the retinal arterioles when administered intraluminally.; identifier:PMID:29966442; 開始ページ : 1374; 終了ページ : 1382
• DOI: info:doi/10.1080/02713683.2018.1496266; https://doi.org/info:doi/10.1080/02713683.2018.1496266
• Persistent ID (NDL): info:ndljp/pid/11378629; https://dl.ndl.go.jp/pid/11378629
• Collection: 障害者向け資料
• Collection (Materials For Handicapped People:1): テキストデータ
• Collection (particular): 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文; https://dl.ndl.go.jp/collections/A00014
• Acquisition Basis: 博士論文（自動収集）
• Date Accepted (W3CDTF): 2019-11-04T14:30:53+09:00
• Format (IMT): application/pdf
• Access Restrictions: 国立国会図書館内限定公開
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• Periodical Title (URI): http://amcor.asahikawa-med.ac.jp/modules/xoonips/detail.php?id=20180928_K526
• Data Provider (Database): 国立国会図書館 : 国立国会図書館デジタルコレクション; https://dl.ndl.go.jp