Kurachi Y, Ito H, Sugimoto T, Shimizu T, Miki I, Ui M
2nd Department of Internal Medicine, University of Tokyo, Japan.
Pflugers Arch. 1989 May;414(1):102-4. doi: 10.1007/BF00585635.
Phenylephrine (10 microM), added in the bathing solution, stimulated the cardiac muscarinic K+ channel (IK.ACh) in the cell-attached patch. The pipette solution contained 10 microM atropine and 100 microM theophylline to block the muscarinic acetylcholine and adenosine receptors, respectively. The channel activation induced by phenylephrine was blocked by prazosin, an alpha 1-antagonist, indicating that alpha 1-adrenergic receptor mediates the response. Phenylephrine-induced activation was prevented by nordihydroguaiaretic acid, a lipoxygenase inhibitor, and AA-861, a 5-lipoxygenase inhibitor, but was not affected by indomethacin, a cyclooxygenase inhibitor. These observations suggest that 5-lipoxygenase metabolites of arachidonic acid may be involved in the alpha-adrenergic activation of IK.ACh.
加入浴液中的去氧肾上腺素（10微摩尔）刺激了细胞贴附式膜片中的心肌毒蕈碱钾通道（IK.ACh）。移液管溶液含有10微摩尔阿托品和100微摩尔茶碱，分别用于阻断毒蕈碱型乙酰胆碱受体和腺苷受体。去氧肾上腺素诱导的通道激活被α1拮抗剂哌唑嗪阻断，表明α1肾上腺素能受体介导了该反应。去氧肾上腺素诱导的激活被脂氧合酶抑制剂去甲二氢愈创木酸和5-脂氧合酶抑制剂AA-861所抑制，但不受环氧化酶抑制剂吲哚美辛的影响。这些观察结果表明，花生四烯酸的5-脂氧合酶代谢产物可能参与了IK.ACh的α-肾上腺素能激活过程。
