アゴニスト誘発性血管平滑筋収縮には1型イノシトール3リン酸受容体サブタイプが主に関与する
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- 中村 健
- 順天堂大・医・第二生理 科学技術振興機構・国際・カルシウム振動プロジェクト
書誌事項
- タイトル別名
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- Primary role of inositol 1,4,5-trisphosphate receptor type 1 in agonist-induced aortic contraction in mice
抄録
Contraction of vascular smooth muscles is under the regulation of sympathetic activity and vasoactive hormones. It is known that release of Ca2+ from inositol 1,4,5-trisphosphate (IP3)-sensitive stores causes the initial phase of agonist-induced vasocontraction. In the present study, phenylephrine (PE)-induced contraction was measured in thoracic aortas isolated from the wild-type (WT) and IP3 receptor type 1 knockout (IP3R1-KO) mice, in order to specify the IP3 receptor subtype responsible for the agonist-induced contraction. PE (10−8–10−6 M)-induced aortic contraction in the IP3R1-KO mice was greatly diminished, compared to that in WT mice, and lacked the steep contraction which was invariably seen in WT aortas immediately after PE application at 10−6 M. But, high K+-induced contraction was indistinguishable between WT and IP3R1-KO aortas. Immunoblotting analysis demonstrated the presence of three IP3 receptor subtypes (IP3R1, IP3R2 and IP3R3) in WT mouse thoracic aorta; however, abundance of each subtype was in the order of IP3R1 > IP3R3 >> IP3R2. These results indicate that IP3R1 constitutes the Ca2+ release channels critical to vasocontraction regulated by sympathetic activity and vasoactive hormones. [J Physiol Sci. 2006;56 Suppl:S42]
収録刊行物
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- 日本生理学会大会発表要旨集
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日本生理学会大会発表要旨集 2006 (0), 042-042, 2006
一般社団法人 日本生理学会
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- CRID
- 1390001205728932224
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- NII論文ID
- 130005448130
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- JaLC
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