Lebrun P, Fang Z Y, Antoine M H, Herchuelz A, Hermann M, Berkenboom G, Fontaine J
Laboratory of Pharmacology, Faculty of Medicine and Pharmacy, Brussels Free University, Belgium.
Pharmacology. 1990;41(1):36-48. doi: 10.1159/000138697.
Cromakalim, pinacidil and nitroprusside provoked concentration-dependent relaxations of K(+)-depolarized rat aortae. Glibenclamide, tolbutamide and to a lesser extent tetraethylammonium antagonized the vasorelaxant action of cromakalim and pinacidil. Cromakalim, pinacidil but not nitroprusside elicited a marked increase in 86Rb outflow from preloaded and perifused aortic rings. These increases in 86Rb outflow were inhibited in a concentration-dependent manner by glibenclamide and tetraethylammonium. Our data extend previous observations indicating the involvement of K+ channels in the vasorelaxant properties of cromakalim and pinacidil. Moreover, the present findings suggest that both compounds could interfere with a vascular type of ATP-sensitive K+ channels.
克罗卡林、吡那地尔和硝普钠可引起钾离子去极化的大鼠主动脉产生浓度依赖性舒张。格列本脲、甲苯磺丁脲以及程度较轻的四乙铵可拮抗克罗卡林和吡那地尔的血管舒张作用。克罗卡林、吡那地尔可引起预先装载并灌流的主动脉环中86Rb流出量显著增加，但硝普钠无此作用。格列本脲和四乙铵可浓度依赖性地抑制这些86Rb流出量的增加。我们的数据扩展了先前的观察结果，表明钾离子通道参与了克罗卡林和吡那地尔的血管舒张特性。此外，目前的研究结果表明，这两种化合物可能会干扰血管类型的ATP敏感性钾离子通道。
