Zhao Juan, Ma Hui-Jie, Teng Xu, Wang Qing-Shan
Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang 050017, China.
Sheng Li Xue Bao. 2004 Jun 25;56(3):369-73.
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.
采用细胞内微电极技术研究了一氧化氮（NO）对兔房室（AV）结细胞自发活动的电生理效应。结果如下：（1）NO供体硝普钠（SNP，1~1000 μmol/L）和3-吗啉代辛二酰亚胺（SIN-1，100、1000 μmol/L）以浓度依赖的方式降低动作电位幅度（APA）、自发放电频率（RSF）、舒张期（4期）去极化速度（VDD）和最大去极化速度（V(max)）。（2）用L型钙通道激动剂Bay K8644（0.25 μmol/L）预处理可完全逆转SNP（100 μmol/L）对AV结细胞的作用。（3）灌流液中Ca(2+)浓度升高（5 mmol/L）可拮抗SNP对AV结细胞的作用。（4）用无Ca(2+)的K-H溶液灌流可完全消除SNP对AV结细胞的作用。（5）应用鸟苷酸环化酶抑制剂亚甲蓝（50 μmol/L）不能消除SNP（100 μmol/L）的抑制作用。所有这些结果表明，NO对兔AV结细胞的自发活动有负性作用。这些作用可能是由于通过一种不依赖cGMP的机制减少钙内流所致。
