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Kokyu to Junkan Volume 38, Issue 10 （October 1990）

呼吸と循環 38巻10号（1990年10月発行）

Japanese English

研究

ラット胸部大動脈における内皮由来血管収縮因子（EDCF）と内皮由来血管弛緩因子（EDRF）の役割—EDCFの本体の解明 The role of endothelium-derived contracting factor (EDCF) and endothelium-derived relaxing factor (EDRF) in the aorta of the rat:Identification of EDCF 伊藤隆之 ¹ , 加藤敏夫 ¹ , 岩間芳生 ¹ , 村松雅人 ¹ , 奥村健二 ¹ , 橋本秀和 ¹ , 佐竹辰夫 ¹ , 小川宏一 ² Takayuki Ito ¹ , Toshio Kato ¹ , Yoshio Iwama ¹ , Masahito Muramatsu ¹ , Kenji Okumura ¹ , Hidekazu Hashimoto ¹ , Tatsuo Satake ¹ , Kouichi Ogawa ² ¹名古屋大学医学部第二内科 ²名城病院 ¹The 2nd Department of Internal Medicine, Nagoya University School of Medicine ²Meijo Hospital キーワード：内皮由来血管収縮因子（endothelium-derived Contracting factor） , 内皮由来血管弛緩因子（endothelium-derived relaxing factor） , プロスタグランジンH₂（prostaglandin H₂） Keyword: 内皮由来血管収縮因子（endothelium-derived Contracting factor） , 内皮由来血管弛緩因子（endothelium-derived relaxing factor） , プロスタグランジンH₂（prostaglandin H₂） pp.1001-1007

発行日 1990年10月15日 Published Date 1990/10/15

DOI https://doi.org/10.11477/mf.1404910028

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Abstract 文献概要
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　血管平滑筋における内皮由来血管収縮因子（EDCF）および内皮由来血管弛緩因子（EDRF）の関与の程度をSHR,WKYの胸部大動脈輪状標本を用い調べ，さらに，EDCFの本体を追求した。①SHRとWKY群間のEDRF産生の程度には差はなく，SHRではWKYに比べEDCFの産生亢進がみられることが示唆された。②EDCFの産生は，TXA₂　inhibitorでは抑制を受けず，TXA₂／PGH₂　antagonistによって抑制されることを初めて見いだした。③Acetylcholine刺激時にはPGI₂，PGE₂の産生増加がみられ，PGF_2α，TXA₂の増加はみられなかった。④外因性PGH₂，TXA₂，PGF_2αはSHRの大動脈を低濃度より収縮させた。⑤産生されたPG濃度と薬理作用を発現させる濃度を比較し，precursorであるPGH₂がEDCFの本体であることを示唆した。

The present experiment was performed to identify endothelium-derived contracting factor produced by acetylcholine stimulation in the aorta of spontaneo-usly hypertensive rats (SHR) and normotensive Wi-star-Kyoto rats (WKY). The rings of the thoracic aorta were obtained from age-matched SHR and WKY, and changes in isometric tension were record-ed. The relaxant responses to acetylcholine in the rings from SHR were significantly weaker than those obtained in WKY. The relaxant responses to acety-lcholine were significantly enhanced by pretreatment with a cyclooxygenase-inhibitor (indomethacin) or thromboxane A₂/prostaglandin H₂ receptor antagon-ist (ONO-3708) both in the SHR and WKY rings. A thromboxane A₂ synthetase inhibitor (OKY-046) did not affect the acetylcholine-induced relaxation in therings from SHR or WKY. In the organ bath solu-tion, following acetylcholine stimulation, prostaglan-din E₂ and 6-keto-prostaglandin F_1α, concentrations increased, but prostaglandin F_2α and thromboxane B₂ concentrations did not increase. Exogenous prosta-glandin H₂, a stable analogue of thromboxane A₂ (STA₂) and prostaglandin F_2α induced contractions of the SHR rings at a lower concentration than pro-staglandin E₂, prostaglandin D₂ and prostaglandin I₂. These contractile responses to various prostaglandins were markedly inhibited by pretreatment with ONO-3708. A prostacyclin synthetase inhibitor did not af-fect the relaxant responses to acetylcholine in the SHR rings.

These results show that endothelium-derived con-tracting factor is produced and released by acetylcho-line stimulation not only in the aorta of SHR but also in that of WKY. The results also suggest that pro-staglandin H₂, a precursor of the released prostaglan-dins, is a strong candidate for endothelium-derived contracting factor produced by acetylcholine stimula-tion.