Höhn József, Pataricza János, Petri András, Tóth Gábor K, Balogh Adám, Varró András, Papp Julius Gy
Department of Surgery, Albert Szent-Györgyi Medical Center, University of Szeged, Hungary.
Basic Clin Pharmacol Toxicol. 2004 Jun;94(6):271-3. doi: 10.1111/j.1742-7843.2004.pto940603.x.
The involvement of potassium channels in the venodilating capacity of the inodilator levosimendan in human saphenous vein preparations was investigated. Levosimendan caused relaxation with 50% effective concentration (EC50) of 0.32 +/- 0.04 microM in isolated veins contracted by 5-hydroxytryptamine. Fifteen microM glibenclamide, a blocker of the ATP-sensitive potassium channels (K(ATP)), partially inhibited the relaxing effect of the inodilator. In the presence of iberiotoxin, the selective blocker of large conductance calcium-activated potassium channels (BK(Ca)), levosimendan induced contraction with EC50 of 0.21 +/- 0.06 microM. We presume that levosimendan dilates human saphenous veins by interacting with hyperpolarizing potassium channels (K(ATP) and BK(Ca)).
研究了钾通道在血管扩张剂左西孟旦对人隐静脉制剂的血管舒张能力中的作用。左西孟旦在由5-羟色胺收缩的离体静脉中引起舒张,其50%有效浓度(EC50)为0.32±0.04微摩尔。15微摩尔格列本脲,一种ATP敏感性钾通道(K(ATP))阻滞剂,部分抑制了血管扩张剂的舒张作用。在大电导钙激活钾通道(BK(Ca))的选择性阻滞剂iberiotoxin存在下,左西孟旦诱导收缩,EC50为0.21±0.06微摩尔。我们推测左西孟旦通过与超极化钾通道(K(ATP)和BK(Ca))相互作用来舒张人隐静脉。