Electrophysiological effects of nitric oxide on spontaneous activity of rabbit atrioventricular node cells
Zhao Juan, Ma Huijie, Teng Xu, Wang Qingshan
Department of Physiology, Institute of Basic Medicine, Hebei Medical University. Shijiazhuang 050017, China
Abstract
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 #mu#mol/L) and 3-morpholinosydnonimine (SIN-l, 100, 1000 #mu#mol/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 (Vmax) in a concentration-dependent manner. (2) Pretreatment with L-type calcium channel agonist Bay K8644 (0.25 #mu#mol/L) completely reversed the effects of SNP (100 #mu#mol/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 #mu#mol/L), a guanylyl cyclase inhibitor, failed to abolish the inhibitory effects of SNP (100 #mu#mol/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.
Key words: Nitric oxide;Atrioventricular node;Calcium currents;Electrophysiology
Received: Accepted:
Corresponding author: E-mail:
Citing This Article:
Zhao Juan, Ma Huijie, Teng Xu, Wang Qingshan. Electrophysiological effects of nitric oxide on spontaneous activity of rabbit atrioventricular node cells. Acta Physiol Sin 2004; 56 (3): (in Chinese with English abstract).