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

• 資料種別: 博士論文
• ISSN: 0271-3683
• タイトル: Thrombin-Induced Responses Via Protease-Activated Receptor 1 Blocked by the Endothelium on Isolated Porcine Retinal Arterioles
• 巻次・部編番号: 43 11
• 著者・編者: 髙橋, 賢伍
• 出版年月日等: 2018-11
• 出版年（W3CDTF）: 2018-11
• タイトル（掲載誌）: Current eye research
• 授与機関名: 旭川医科大学
• 授与年月日: 2018-09-28
• 授与年月日（W3CDTF）: 2018-09-28
• 報告番号: 甲第526号
• 学位: 博士（医学）
• 博論授与番号: 甲第526号
• 本文の言語コード: eng
• 件名標目: PAR-1; Thrombin; endothelium blood retinal barrier; protease-activated receptor 1; vasoconstriction; vasorelaxation
• 一般注記: 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
• 国立国会図書館永続的識別子: info:ndljp/pid/11378629; https://dl.ndl.go.jp/pid/11378629
• コレクション（共通）: 障害者向け資料
• コレクション（障害者向け資料：レベル1）: テキストデータ
• コレクション（個別）: 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
• 収集根拠: 博士論文（自動収集）
• 受理日（W3CDTF）: 2019-11-04T14:30:53+09:00
• 記録形式（IMT）: application/pdf
• オンライン閲覧公開範囲: 国立国会図書館内限定公開
• デジタル化資料送信: 図書館・個人送信対象外
• 遠隔複写可否（NDL）: 可
• 掲載誌（URI）: http://amcor.asahikawa-med.ac.jp/modules/xoonips/detail.php?id=20180928_K526
• 連携機関・データベース: 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