WEKO3
アイテム
{"_buckets": {"deposit": "944e258a-5b06-4f3c-a074-084f4e5a3e4f"}, "_deposit": {"created_by": 3, "id": "19114", "owners": [3], "pid": {"revision_id": 0, "type": "depid", "value": "19114"}, "status": "published"}, "_oai": {"id": "oai:twinkle.repo.nii.ac.jp:00019114", "sets": ["1985"]}, "author_link": ["298084", "298083", "298086", "298085"], "item_10001_alternative_title_1": {"attribute_name": "別タイトル", "attribute_value_mlt": [{"subitem_alternative_title": "新規1,4ベンゾチアゼピン誘導体K201のラット大動脈平滑筋の細胞内Caと収縮への効果"}]}, "item_10001_biblio_info_7": {"attribute_name": "書誌情報", "attribute_value_mlt": [{"bibliographicIssueDates": {"bibliographicIssueDate": "2004-01", "bibliographicIssueDateType": "Issued"}, "bibliographicIssueNumber": "1", "bibliographicPageEnd": "46", "bibliographicPageStart": "39", "bibliographicVolumeNumber": "74", "bibliographic_titles": [{"bibliographic_title": "東京女子医科大学雑誌"}]}]}, "item_10001_creator_2": {"attribute_name": "著者名", "attribute_type": "creator", "attribute_value_mlt": [{"creatorNames": [{"creatorName": "SHIMAMOTO, Ken"}], "nameIdentifiers": [{"nameIdentifier": "298083", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "KANEKO, Noboru"}], "nameIdentifiers": [{"nameIdentifier": "298084", "nameIdentifierScheme": "WEKO"}]}]}, "item_10001_date_25": {"attribute_name": "受付日付", "attribute_value_mlt": [{"subitem_date_issued_datetime": "2010-08-10", "subitem_date_issued_type": "Created"}]}, "item_10001_description_5": {"attribute_name": "抄録", "attribute_value_mlt": [{"subitem_description": "1,4ベンゾチアゼピン誘導体K201 (JTV519)は心筋保護を目的に新規合成された.心筋ではナトリウム,カリウム,カルシウムチャンネルの阻害作用があり,抗虚血,抗不整脈作用を有する.この研究ではラット大動脈を用いて, K201の平滑筋の細胞内カルシウムと収縮への作用を検討した.細胞内カルシウム測定には蛍光指示薬furaPE3/AMと放射性カルシウム45(45 Ca)を用いた.カルシウム除去液では, 10-6Mノルエピネフリンによる収縮は持続性であるが,カルシウムトランジエント([Ca2+]i)は一過性であった.この収縮と[Ca2+]iは10-5M K201の前投与により消失した. 72.7mM高濃度カリウムによる収縮を10-5\u003eM K201は100%抑制するが, [Ca2+]iは約20%が残存した.この残存した[Ca2+]iは10-5Mベラパミルで消失した.高濃度カリウムによる脱分極では, 10-4M K201の前投与による^\u003c45\u003eCaの流入の抑制は34%で, 10-5Mジルチアゼムによる抑制は85%であった. 10-4M K201と10-5Mジルチアゼムはほぼ完全に高濃度カリウムによる収縮を抑制した. K201の血管平滑筋収縮抑制への作用機序としてCaチャンネル拮抗作用,α受容体阻害作用では十分に説明できず, Ca感受性を変える細胞内Ca拮抗作用が推測される.", "subitem_description_type": "Abstract"}, {"subitem_description": "The 1,4-benzothiazepine derivative K201 (synonym JTV519) was newly synthesized for use as a cardioprotective agent. This study was conducted to examine the effects of K201 on rat aortic smooth muscle contraction and the mobilization of intracellular Ca2+. Intracellular Ca2+ level was determined using a fluorescent Ca2+ indicator furaPE3 and 45Ca2+. Norepinephrine induced transient contraction and an increase in calcium transient ([Ca2+]i) under Ca2+-free conditions in isolated rat aorta smooth muscle samples. Pretreatment with K201 at 10-5 M inhibited the contraction and increase of [Ca2+]i induced by norepinephrine at 10-6 M. K201 at 10-5 M almost completely inhibited the vascular smooth muscle contraction induced by high potassium (K+), although approximately 20% of calcium transient remained. Addition of 10-5 M verapamil almost completely inhibited the resting [Ca2+]i. [Ca2+]i-tension relationship was examined at various doses of K201 and diltiazem in rat aorta stimulated by high K+. Both muscle tension and [Ca2+]i decreased by K201 dose-dependently, greater relaxation was induced by K201 than by diltiazem at the same resting level of [Ca2+]i. In high K+-induced depolarization, pretreatment with K201 at 10-4 M inhibited 45 Ca2+ influx by 34%, while diltiazem at 10-5 M inhibited the influx by 85%. In addition to a mild α-adrenoceptor and Ca2+ -channel blocking activity, K201 may alter the Ca2+ sensitivity of intracellular contractile elements.", "subitem_description_type": "Abstract"}]}, "item_10001_full_name_3": {"attribute_name": "著者別名", "attribute_value_mlt": [{"nameIdentifiers": [{"nameIdentifier": "298085", "nameIdentifierScheme": "WEKO"}], "names": [{"name": "島本, 健"}]}, {"nameIdentifiers": [{"nameIdentifier": "298086", "nameIdentifierScheme": "WEKO"}], "names": [{"name": "金子, 昇"}]}]}, "item_10001_publisher_8": {"attribute_name": "出版者", "attribute_value_mlt": [{"subitem_publisher": "東京女子医科大学学会"}]}, "item_10001_source_id_11": {"attribute_name": "NCID", "attribute_value_mlt": [{"subitem_source_identifier": "AN00161368", "subitem_source_identifier_type": "NCID"}]}, "item_10001_source_id_9": {"attribute_name": "ISSN", "attribute_value_mlt": [{"subitem_source_identifier": "0040-9022", "subitem_source_identifier_type": "ISSN"}]}, "item_10001_subject_47": {"attribute_name": "著者キーワード", "attribute_value_mlt": [{"subitem_subject": "K201 (JTV519)", "subitem_subject_scheme": "Other"}, {"subitem_subject": "Ca2+-channel blocker", "subitem_subject_scheme": "Other"}, {"subitem_subject": "Ca2+ sensitivity", "subitem_subject_scheme": "Other"}, {"subitem_subject": "smooth muscle", "subitem_subject_scheme": "Other"}, {"subitem_subject": "furaPE3", "subitem_subject_scheme": "Other"}, {"subitem_subject": "AM", "subitem_subject_scheme": "Other"}]}, "item_10001_text_35": {"attribute_name": "著者所属", "attribute_value_mlt": [{"subitem_text_value": "Department of Cardiology, Tokyo Women\u0027s Medical University Aoyama Hospital"}, {"subitem_text_value": "Department of Cardiology and Pneumology, Dokkyo University School of Medicine"}, {"subitem_text_value": "東京女子医科大学附属青山病院循環器内科"}, {"subitem_text_value": "獨協医科大学心血管肺内科"}]}, "item_10001_version_type_20": {"attribute_name": "著者版フラグ", "attribute_value_mlt": [{"subitem_version_resource": "http://purl.org/coar/version/c_970fb48d4fbd8a85", "subitem_version_type": "VoR"}]}, "item_files": {"attribute_name": "ファイル情報", "attribute_type": "file", "attribute_value_mlt": [{"accessrole": "open_date", "date": [{"dateType": "Available", "dateValue": "2017-08-22"}], "displaytype": "detail", "download_preview_message": "", "file_order": 0, "filename": "KJ00006018689.pdf", "filesize": [{"value": "794.4 kB"}], "format": "application/pdf", "future_date_message": "", "is_thumbnail": false, "licensetype": "license_free", "mimetype": "application/pdf", "size": 794400.0, "url": {"label": "KJ00006018689.pdf", "url": "https://twinkle.repo.nii.ac.jp/record/19114/files/KJ00006018689.pdf"}, "version_id": "161184d0-74d1-46ee-831f-030b7a0a6fd5"}]}, "item_language": {"attribute_name": "言語", "attribute_value_mlt": [{"subitem_language": "eng"}]}, "item_resource_type": {"attribute_name": "資源タイプ", "attribute_value_mlt": [{"resourcetype": "journal article", "resourceuri": "http://purl.org/coar/resource_type/c_6501"}]}, "item_title": "Effects of a Novel 1,4-Benzothiazepine Derivative, K201, on Cytosolic Ca2+ and Contraction in Isolated Smooth Muscle of Rat Aorta", "item_titles": {"attribute_name": "タイトル", "attribute_value_mlt": [{"subitem_title": "Effects of a Novel 1,4-Benzothiazepine Derivative, K201, on Cytosolic Ca2+ and Contraction in Isolated Smooth Muscle of Rat Aorta"}]}, "item_type_id": "10001", "owner": "3", "path": ["1985"], "permalink_uri": "http://hdl.handle.net/10470/26413", "pubdate": {"attribute_name": "公開日", "attribute_value": "2010-08-10"}, "publish_date": "2010-08-10", "publish_status": "0", "recid": "19114", "relation": {}, "relation_version_is_last": true, "title": ["Effects of a Novel 1,4-Benzothiazepine Derivative, K201, on Cytosolic Ca2+ and Contraction in Isolated Smooth Muscle of Rat Aorta"], "weko_shared_id": -1}
Effects of a Novel 1,4-Benzothiazepine Derivative, K201, on Cytosolic Ca2+ and Contraction in Isolated Smooth Muscle of Rat Aorta
http://hdl.handle.net/10470/26413
http://hdl.handle.net/10470/26413e63bef91-d108-4c79-8de1-f507283f18f2
名前 / ファイル | ライセンス | アクション |
---|---|---|
KJ00006018689.pdf (794.4 kB)
|
|
Item type | 学術雑誌論文 / Journal Article(1) | |||||
---|---|---|---|---|---|---|
公開日 | 2010-08-10 | |||||
タイトル | ||||||
タイトル | Effects of a Novel 1,4-Benzothiazepine Derivative, K201, on Cytosolic Ca2+ and Contraction in Isolated Smooth Muscle of Rat Aorta | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
別タイトル | ||||||
その他のタイトル | 新規1,4ベンゾチアゼピン誘導体K201のラット大動脈平滑筋の細胞内Caと収縮への効果 | |||||
著者名 |
SHIMAMOTO, Ken
× SHIMAMOTO, Ken× KANEKO, Noboru |
|||||
著者別名 | ||||||
姓名 | 島本, 健 | |||||
著者別名 | ||||||
姓名 | 金子, 昇 | |||||
出版者 | ||||||
出版者 | 東京女子医科大学学会 | |||||
受付日付 | ||||||
日付 | 2010-08-10 | |||||
日付タイプ | Created | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 0040-9022 | |||||
NCID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AN00161368 | |||||
書誌情報 |
東京女子医科大学雑誌 巻 74, 号 1, p. 39-46, 発行日 2004-01 |
|||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | 1,4ベンゾチアゼピン誘導体K201 (JTV519)は心筋保護を目的に新規合成された.心筋ではナトリウム,カリウム,カルシウムチャンネルの阻害作用があり,抗虚血,抗不整脈作用を有する.この研究ではラット大動脈を用いて, K201の平滑筋の細胞内カルシウムと収縮への作用を検討した.細胞内カルシウム測定には蛍光指示薬furaPE3/AMと放射性カルシウム45(45 Ca)を用いた.カルシウム除去液では, 10-6Mノルエピネフリンによる収縮は持続性であるが,カルシウムトランジエント([Ca2+]i)は一過性であった.この収縮と[Ca2+]iは10-5M K201の前投与により消失した. 72.7mM高濃度カリウムによる収縮を10-5>M K201は100%抑制するが, [Ca2+]iは約20%が残存した.この残存した[Ca2+]iは10-5Mベラパミルで消失した.高濃度カリウムによる脱分極では, 10-4M K201の前投与による^<45>Caの流入の抑制は34%で, 10-5Mジルチアゼムによる抑制は85%であった. 10-4M K201と10-5Mジルチアゼムはほぼ完全に高濃度カリウムによる収縮を抑制した. K201の血管平滑筋収縮抑制への作用機序としてCaチャンネル拮抗作用,α受容体阻害作用では十分に説明できず, Ca感受性を変える細胞内Ca拮抗作用が推測される. | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | The 1,4-benzothiazepine derivative K201 (synonym JTV519) was newly synthesized for use as a cardioprotective agent. This study was conducted to examine the effects of K201 on rat aortic smooth muscle contraction and the mobilization of intracellular Ca2+. Intracellular Ca2+ level was determined using a fluorescent Ca2+ indicator furaPE3 and 45Ca2+. Norepinephrine induced transient contraction and an increase in calcium transient ([Ca2+]i) under Ca2+-free conditions in isolated rat aorta smooth muscle samples. Pretreatment with K201 at 10-5 M inhibited the contraction and increase of [Ca2+]i induced by norepinephrine at 10-6 M. K201 at 10-5 M almost completely inhibited the vascular smooth muscle contraction induced by high potassium (K+), although approximately 20% of calcium transient remained. Addition of 10-5 M verapamil almost completely inhibited the resting [Ca2+]i. [Ca2+]i-tension relationship was examined at various doses of K201 and diltiazem in rat aorta stimulated by high K+. Both muscle tension and [Ca2+]i decreased by K201 dose-dependently, greater relaxation was induced by K201 than by diltiazem at the same resting level of [Ca2+]i. In high K+-induced depolarization, pretreatment with K201 at 10-4 M inhibited 45 Ca2+ influx by 34%, while diltiazem at 10-5 M inhibited the influx by 85%. In addition to a mild α-adrenoceptor and Ca2+ -channel blocking activity, K201 may alter the Ca2+ sensitivity of intracellular contractile elements. | |||||
著者所属 | ||||||
Department of Cardiology, Tokyo Women's Medical University Aoyama Hospital | ||||||
著者所属 | ||||||
Department of Cardiology and Pneumology, Dokkyo University School of Medicine | ||||||
著者所属 | ||||||
東京女子医科大学附属青山病院循環器内科 | ||||||
著者所属 | ||||||
獨協医科大学心血管肺内科 | ||||||
著者キーワード | ||||||
主題Scheme | Other | |||||
主題 | K201 (JTV519) | |||||
著者キーワード | ||||||
主題Scheme | Other | |||||
主題 | Ca2+-channel blocker | |||||
著者キーワード | ||||||
主題Scheme | Other | |||||
主題 | Ca2+ sensitivity | |||||
著者キーワード | ||||||
主題Scheme | Other | |||||
主題 | smooth muscle | |||||
著者キーワード | ||||||
主題Scheme | Other | |||||
主題 | furaPE3 | |||||
著者キーワード | ||||||
主題Scheme | Other | |||||
主題 | AM |