Li X T, Duan H R, He R R
Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang 050017, China.
Acta Pharmacol Sin. 2000 Oct;21(10):931-5.
To study the effects of agmatine on spontaneous activity of atrioventricular (AV) node and its action mechanisms.
Action potentials in AV node cells were recorded using intracellular microelectrode technique.
Agmatine not only reduced the amplitude of action potential (APA), maximal rate of depolarization (Vmax), velocity of diastolic (phase 4) depolarization (VDD), and rate of spontaneous firing (RSF), but also prolonged 90% duration of action potential (APD90) in a concentration-dependent manner. The effects of agmatine (10 mmol/L) could be blocked completely by pretreatment with idazoxan (0.1 mmol/L), an imidazoline receptor (IR) and alpha 2-adrenergic receptor (alpha 2-AR) antagonist. Pretreatment with NG-nitro-L-arginine methyl ester (L-NAME, 0.5 mmol/L), a nitric oxide (NO) synthase inhibitor, did not affect the effects of agmatine on AV node cells. Elevation of Ca2+ concentration (5 mmol/L) in perfusate antagonized the effects of agmatine (10 mmol/L). Lemakalim (30 mumol/L), an ATP-sensitive potassium channel opener, inhibited the prolonging effects of agmatine on repolarization.
The inhibitory effects of agmatine on spontaneous activity of AV node cells in rabbits were likely mediated by IR and/or alpha 2-AR, and were related to the reduction in calcium influx and potassium efflux.
研究胍丁胺对房室结自发活动的影响及其作用机制。
采用细胞内微电极技术记录房室结细胞的动作电位。
胍丁胺不仅以浓度依赖的方式降低动作电位幅度（APA）、最大去极化速率（Vmax）、舒张期（4期）去极化速度（VDD）和自发放电频率（RSF），还延长动作电位90%时程（APD90）。胍丁胺（10 mmol/L）的作用可被咪唑啉受体（IR）和α2-肾上腺素能受体（α2-AR）拮抗剂伊达唑啉（0.1 mmol/L）预处理完全阻断。一氧化氮（NO）合酶抑制剂NG-硝基-L-精氨酸甲酯（L-NAME，0.5 mmol/L）预处理不影响胍丁胺对房室结细胞的作用。灌流液中Ca2+浓度升高（5 mmol/L）可拮抗胍丁胺（10 mmol/L）的作用。ATP敏感性钾通道开放剂莱马卡林（30 μmol/L）抑制胍丁胺对复极化的延长作用。
胍丁胺对兔房室结细胞自发活动的抑制作用可能由IR和/或α2-AR介导，且与钙内流减少和钾外流有关。
