Electrophysiological effects of hydrogen sulfide on pacemaker cells in sinoatrial nodes of rabbits.
- Author:
Meng XU
1
;
Yu-Ming WU
;
Qian LI
;
Xin WANG
;
Rui-Rong HE
Author Information
1. Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang 050017, China.
- Publication Type:Journal Article
- MeSH:
Action Potentials;
Animals;
Glyburide;
pharmacology;
Hydrogen Sulfide;
pharmacology;
Microelectrodes;
Myocytes, Cardiac;
cytology;
drug effects;
Rabbits;
Sinoatrial Node;
cytology;
Sulfides;
pharmacology
- From:
Acta Physiologica Sinica
2008;60(2):175-180
- CountryChina
- Language:English
-
Abstract:
The cardiac electrophysiological effects of hydrogen sulfide (H(2)S) on pacemaker cells in sinoatrial (SA) nodes of rabbits were examined using intracellular microelectrode technique. The results obtained were as follows: (1) The velocity of diastolic (phase 4) depolarization (VDD) and rate of pacemaker firing (RPF) in normal pacemaker cells in SA nodes were decreased by NaHS (H(2)S donor) (50, 100, 200 μmol/L) in a concentration-dependent manner; (2) ATP-sensitive K(+) (K(ATP)) channel blocker glybenclamide (Gli, 20 μmol/L) blocked the effect of NaHS (100 μmol/L) on pacemaker cells; (3) Pretreatment with CsCl (2 mmol/L), a blocker of pacemaker current (I(f)), did not affect the effect of NaHS (100 μmol/L) on SA node pacemaker cells; (4) DL-propargylglycine (PPG, 200 μmol/L), an inhibitor of cystathionine γ-lyase (CSE), did not affect the parameters of action potentials in pacemaker cells in SA nodes. All these results suggest that H(2)S exerts a negative chronotropic action on pacemaker cells in SA nodes of rabbits. These effects are likely due to an increase in potassium efflux through opening K(ATP) channels; I(f)is unlikely to play a major role in these effects. In our study, there was no evidence for the generation of endogenous H(2)S by CSE in SA node pacemaker cells.
