Electrophysiological effects of nitric oxide on spontaneous activity of rabbit atrioventricular node cells.
- Author:
Juan ZHAO
1
;
Hui-Jie MA
;
Xu TENG
;
Qing-Shan WANG
Author Information
1. Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang 050017, China.
- Publication Type:Journal Article
- MeSH:
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester;
pharmacology;
Action Potentials;
drug effects;
Animals;
Atrioventricular Node;
cytology;
physiology;
Calcium;
metabolism;
Calcium Channel Agonists;
pharmacology;
Calcium Channels, L-Type;
metabolism;
Depression, Chemical;
Female;
Male;
Microelectrodes;
Nitric Oxide;
physiology;
Rabbits
- From:
Acta Physiologica Sinica
2004;56(3):369-373
- CountryChina
- Language:English
-
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 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.
