辣椒素对家兔房室结细胞自发活动的电生理效应(英文)

Electrophysiological effects of capsaicin on spontaneous activity of rabbit atrioventricular node cells

本工作旨在研究辣椒素对家兔房室结细胞自发活动的电生理效应及其用机制。应用经典玻璃微电极记录方法,观察到辣椒素(1-30μmol/L)剂量依赖性地抑制房室结起搏细胞的动作电位幅度,零相最大上升速度(Vmax),舒张期除极速度和起搏放电频率,而且延长复极化90％时间(APD90)。应用L型钙通道开放剂Bay K8644(0.5μtmol/L),以及提高灌流液中钙离子浓度(5 mmol/L),均可抑制辣椒素对起搏细胞的电生理效应。辣椒素受体阻断剂钌红(10 μmol/L)对辣椒素(10μmol/L)的上述电生理效应并无影响。上述结果表明,辣椒素能抑制家兔房室结的自发活动,此效应可能与其抑制钙离子内流有关,但并非由辣椒素受体介导。

To study the electrophysiological effects of capsaicin on spontaneous activity of rabbit atrioventricular (AV) node cells, parameters of action potential in AV node were recorded using intracellular microelectrode technique. Capsaicin (1-30 μmol/L) not only decreased the amplitude of action potential, maximal rate of depolarization (Vmax), velocity of diastolic (phase 4) depolarization, and rate of pacemaker firing, but also prolonged the duration of 90% repolarization of action potential (APD90) in a concentration-dependent manner. Both application of L-type Ca2+ channel agonist Bay K8644 (0.5 μmol/L) and elevation of calcium concentration (5 mmol/L) in superfusate antagonized the effects of capsaicin on pacemaker cells. Pretreatment with ruthenium red (10μ,mol/L), a capsaicin receptor blocker, did not affect the effects of capsaicin on AV node cells. Capsaicin exerted an inhibitory action on spontaneous activity of AV node cells in rabbits. These effects were likely due to reduction in calcium influx, but were not mediated by VR1.