Kurachi Y, Nakajima T, Ito H, Sugimoto T
2nd Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
Eur J Pharmacol. 1989 Jun 20;165(2-3):319-22. doi: 10.1016/0014-2999(89)90729-2.
AN-132, a newly developed anti-arrhythmic agent, effectively depressed the acetylcholine (ACh)-induced K+ current (IK.ACh), as measured with the tight-seal, whole-cell clamp technique in single atrial cells of guinea-pig. When GTP-gamma S was loaded into the cell through a pipette, IK.ACh was activated persistently, probably due to irreversible activation of G proteins by GTP-gamma S. AN-132 was much less potent to depress IK.ACh in GTP-gamma S-loaded cells than in GTP-loaded cells. In conclusion, AN-132 may block mainly the cardiac muscarinic ACh receptors to suppress IK.ACh.
AN - 132是一种新研发的抗心律失常药物,在豚鼠单个心房细胞中,采用紧密密封全细胞膜片钳技术测量发现,它能有效抑制乙酰胆碱(ACh)诱导的钾电流(IK.ACh)。当通过移液管将GTP - γ S导入细胞时,IK.ACh被持续激活,这可能是由于GTP - γ S对G蛋白的不可逆激活所致。与导入GTP的细胞相比,AN - 132对导入GTP - γ S的细胞中IK.ACh的抑制作用要弱得多。总之,AN - 132可能主要通过阻断心脏毒蕈碱型ACh受体来抑制IK.ACh。