Saito K, Sakai K
Central Research Laboratories, Chugai Pharmaceutical Co, Ltd., Tokyo, Japan.
Fundam Clin Pharmacol. 1998;12(1):37-43. doi: 10.1111/j.1472-8206.1998.tb00921.x.
The effect of nicorandil on systemic blood pressure (SBP) and heart rate (HR) responses to adenosine was compared with that of cromakalim, an adenosine triphosphate (ATP)-sensitive K+ channel opener, in anesthetized rats. Intravenous (i.v.) adenosine in doses of 1-100 micrograms/kg elicited dose-dependent decreases in SBP, accompanied by decreases in HR. Potentiation of adenosine action by i.v. infusion of either nicorandil (10 or 30 micrograms/kg per min) or cromakalim (0.1 microgram/kg per min) occurred in all of the animals tested. After i.v. treatment with glibenclamide (20 mg/kg), an ATP-sensitive K+ channel blocker, not only adenosine action but also the enhancement of adenosine action by nicorandil and cromakalim were significantly attenuated. The present result indicates that the enhancement of the adenosine action by nicorandil and cromakalim appears to occur at least partly through ATP-sensitive K+ channel activation.
在麻醉大鼠中，比较了尼可地尔与三磷酸腺苷（ATP）敏感性钾通道开放剂克罗卡林对腺苷引起的全身血压（SBP）和心率（HR）反应的影响。静脉注射（i.v.）剂量为1 - 100微克/千克的腺苷可引起SBP呈剂量依赖性下降，并伴有HR下降。在所有受试动物中，静脉输注尼可地尔（10或30微克/千克每分钟）或克罗卡林（0.1微克/千克每分钟）均可增强腺苷的作用。在用ATP敏感性钾通道阻滞剂格列本脲（20毫克/千克）静脉治疗后，不仅腺苷的作用，而且尼可地尔和克罗卡林对腺苷作用的增强均显著减弱。目前的结果表明，尼可地尔和克罗卡林对腺苷作用的增强似乎至少部分是通过ATP敏感性钾通道激活实现的。
