Li X T, Fan Z Z, He R R
Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang 050017, China.
Zhongguo Yao Li Xue Bao. 1999 Oct;20(10):897-901.
To study the electrophysiologic effects of agmatine (Agm) on pacemaker cells in sinoatrial (SA) node.
Parameters of action potential (AP) in SA node were recorded using intracellular microelectrode technique.
Agm not only slowed down the amplitude of action potential (APA), maximal rate of depolarization (Vmax), velocity of diastolic (phase 4) depolarization (VDD), and rate of pacemaker firing (RPF), but also prolonged 90% duration of action potential (APD90) in a concentration-dependent manner. The effects of Agm (10 mmol.L-1) could be blocked completely by pretreatment with idazoxan (0.15 mmol.L-1), an alpha 2-adrenergic receptor (alpha 2-AR) and imidazoline receptor (IR) antagonist. Pretreatment with NG-nitro-L-arginine methyl ester (L-NAME, 1 mmol.L-1), an NOS inhibitor, did not affect the electrophysiologic effects of Agm on pacemaker cells in SA node. Elevation of Ca2+ concentration (5 mmol.L-1) in perfusate antagonized the effects of Agm (10 mmol.L-1). Lemakalim (Lem, 30 mumol.L-1), an opener of ATP-sensitive potassium channels, partially inhibited the prolonging effect of Agm on repolarization.
The electrophysiologic effects of Agm on pacemaker cells in SA node were likely attributed to the reduction in calcium influx and potassium efflux and mediated by alpha 2-AR and IR.
研究胍丁胺(Agm)对窦房结起搏细胞的电生理效应。
采用细胞内微电极技术记录窦房结动作电位(AP)参数。
Agm不仅使动作电位幅度(APA)、最大去极化速率(Vmax)、舒张期(4期)去极化速度(VDD)和起搏发放频率(RPF)减慢,还以浓度依赖方式延长动作电位90%时程(APD90)。α2-肾上腺素能受体(α2-AR)和咪唑啉受体(IR)拮抗剂咪唑克生(0.15 mmol.L-1)预处理可完全阻断Agm(10 mmol.L-1)的效应。一氧化氮合酶(NOS)抑制剂NG-硝基-L-精氨酸甲酯(L-NAME,1 mmol.L-1)预处理不影响Agm对窦房结起搏细胞的电生理效应。灌流液中Ca2+浓度升高(5 mmol.L-1)可拮抗Agm(10 mmol.L-1)的效应。ATP敏感性钾通道开放剂雷马卡林(Lem,30 μmol.L-1)部分抑制Agm对复极化的延长作用。
Agm对窦房结起搏细胞的电生理效应可能归因于钙内流和钾外流减少,且由α2-AR和IR介导。