一氧化氮对家兔房室结细胞自发活动的电生理效应

应用经典玻璃微电极技术,观察一氧化氮(NO)对家兔房室结细胞自发活动的电生理效应及其作用机制。结果显示：(1)NO供体硝普(SNP,1-1000μmol／L)及SIN-1(100,1000μmol／L)剂量依赖性地抑制房室结细胞的动作电位幅值(APA)、零相最大人士升速度(Vmax)、4期自动除极速度(VDD)及自发放电频率(RSF);(2)应用L型钙通道开放剂Bay K8644(0．25μmol／L),可拮抗SNP对房室结细胞的电生理效应;(3)提高灌流液中钙离子浓度(5mmol／L)也可逆转SNP对起搏细胞的抑制效应;(4)用无钙K-H液灌流房室结,可完全阻断SNP对房事结细胞的抑制效应。(5)应用鸟苷酸环化酶阻断剂甲基美蓝(50μmol／L)对SNP的上述电生理效应无影响。以上结果提示,NO可能是通过cGMP非依赖性途径减弱钙离子内流,进而抑制了家兔房室结细胞的自发电活动。

Electrophysiological effects of nitric oxide on spontaneous activity of rabbit atrioventricular node cells

The electrophysiological effects of nitric oxide (NO) on spontaneous activity of rabbit atrioventricular (AV) node cells were examined using intracellular microelectrode technique. The results obtained are as follows. (1) NO donors sodium nitroprusside (SNP, 1~1000 micromol/L) and 3-morpholinosydnonimine (SIN-1, 100, 1000 micromol/L) decreased the amplitude of action potential (APA), rate of spontaneous firing (RSF), velocity of diastolic (phase 4) depolarization (VDD), and maximal rate of depolarization (V(max)) in a concentration-dependent manner. (2) Pretreatment with L-type calcium channel agonist Bay K8644 (0.25 micromol/L) completely reversed the effects of SNP (100 micromol/L) on AV node cells. (3) Elevation of Ca(2+) concentration (5 mmol/L) in superfusate antagonized the effects of SNP on AV node cells. (4) Perfusion with Ca(2+)-free K-H solution, completely abolished the effects of SNP on AV node cells. (5) Application of methylene blue (50 micromol/L), a guanylyl cyclase inhibitor, failed to abolish the inhibitory effects of SNP (100 micromol/L). All these results suggest that NO exerts a negative effect on spontaneous activity of AV node cells in rabbits. These effects are likely due to reduction in calcium influx via a cGMP-independent mechanism.