胍丁胺对人心房纤维的电生理效应。

Electrophysiological effects of agmatine on human atrial fibers.

作者信息

Li X T, He R R, Liu S, Liu L L, Zhang W L, Zhao H, Duan H R

机构信息

Department of Physiology, Hebei Medical University, Shijiazhuang, China.

出版信息

Life Sci. 2000 May 5;66(24):2351-6. doi: 10.1016/s0024-3205(00)00565-8.

DOI:10.1016/s0024-3205(00)00565-8

PMID:10864097

Abstract

The objective of the present study was to study the electrophysiological effects of agmatine on human atrial fibers obtained at cardiac surgery using standard microelectrode techniques. Agmatine (1 to approximately 10 mM) decreased the action potential amplitude (APA), maximum upstroke velocity of phase 0 depolarization (Vmax), velocity of diastolic (phase 4) depolarization (VDD), rate of pacemaker firing (RPF), and action potential duration at 50 and 90% of repolarization (APD(50-90)) in a concentration-dependent manner. Pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME, 0.5 mM), a NOS inhibitor, did not affect the electrophysiological effects of agmatine (5 mM) on human atrial fibers. The effects of agmatine (5 mM) could be blocked completely by pretreatment with idazoxan (0.1 mM), an alpha-2 adrenergic receptor (alpha2-AR) and imidazoline receptor (IR) antagonist. All these results indicate that the effects of agmatine on human atrial fibers are likely due to a decrease of intracellular calcium mediated by IR and/or alpha2-AR.

摘要

本研究的目的是使用标准微电极技术研究胍丁胺对心脏手术中获取的人心房纤维的电生理效应。胍丁胺（1至约10 mM）以浓度依赖性方式降低动作电位幅度（APA）、0期去极化最大上升速度（Vmax）、舒张期（4期）去极化速度（VDD）、起搏发放频率（RPF）以及复极化50%和90%时的动作电位时程（APD(50 - 90)）。用一氧化氮合酶抑制剂N(G)-硝基-L-精氨酸甲酯（L-NAME，0.5 mM）预处理并不影响胍丁胺（5 mM）对人心房纤维的电生理效应。胍丁胺（5 mM）的效应可被α-2肾上腺素能受体（α2-AR）和咪唑啉受体（IR）拮抗剂伊达唑胺（0.1 mM）预处理完全阻断。所有这些结果表明，胍丁胺对人心房纤维的效应可能是由于IR和/或α2-AR介导的细胞内钙减少所致。