WANFANG MED ONLINE

Your Position: Home > Journal List > ACTA PHYSIOLOGICA SINICA > Paper

Electrophysiological effects of hydrogen sulfide on pacemaker cells in sinoatrial nodes of rabbits

( views:58, downloads:0 )

Author:: XU Meng(Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang 050017, China)
WU Yu-Ming(Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang 050017, China)
LI Qian(Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang 050017, China)
WANG Xin(Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang 050017, China)
HE Rui-Rong(Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang 050017, China)

Journal Title:: ACTA PHYSIOLOGICA SINICA

Issue:: Volume 60, Issue 02, 2008

DOI:

Key Word:: electrophysiology; hydrogen sulfide; action potential; sinoatrial node

Abstract： The cardiac electrophysiological effects of hydrogen sulfide (H2S) on pacemaker cells in sinoatrial (SA) nodes of rabbits wereexamined 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 ceils in SA nodes were decreased by NariS (H2S donor)(50, 100, 200 μmol/L) in a concentration-dependent manner; (2) ATP-sensitive K+(KATP) channel blocker glybenclamide (Gli, 20 μmol/L) blocked the effect of NariS (100 μmol/L) on pacemaker cells; (3) Pretreatment with CsC1 (2 mmol/L), a blocker of pacemaker current(If), did not affect the effect of Naris (100 μmol/L) on SA node pacemaker cells; (4) DL-propargylglycine (PPG, 200 μmol/L), aninhibitor of cystathionine γ-lyase (CSE), did not affect the parameters of action potentials in pacemaker cells in SA nodes. All theseresults suggest that H2S exerts a negative chronotropic action on pacemaker cells in SA nodes of rabbits. These effects are likely due toan increase in potassium efflux through opening KATP channels; Ifis unlikely to play a major role in these effects. In our study, there wasno evidence for the generation of endogenous H2S by CSE in SA node pacemaker cells.

Reference

[1]Beauchamp RJ,Bus JS,Popp JA,Boveiko CJ,Andielkovich DA.A critical review of the literature on hydrogen sulfide toxicity.CRC Crit Rev Toxicol 1984; 13:25-97.
[2]Guidotti TL.Hydrogen sulfide.Occup Med 1996; 46:367-371.
[3]Warenycia MW,Goodwin LR,Benishin CG,Reiffenstein Rl,Francom DM,Taylor JD,Dieken FP.Acute hydrogen sulfide poisoning:demonstration of selective uptake of sulfide by the brain stem by measurement of brain sulfide levels.Biochem Pharmacol 1989; 38:973-981.
[4]Wang R.Two's company,three's a crowd:can H2S be the third endogenous gaseous transmitter? FASEB J 2002; 16:1792-1798.
[5]Zhao WM,Zhang J,Lu YJ,Wang R.The vasorelaxant effect of H2S as a novel endogenous gaseous KATP channel opener.EMBO J 2001; 20:6008-6016.
[6]Zhao WM,Wang R.H2S-induced vasorelaxation and underlying cellular and molecular mechanisms.Am J Physiol 2002; 283:H474-H480.
[7]Gross GJ,Fryer RM.Sarcolemmal versus mitochondrial ATPsensitive K+ channels and myocardial preconditioning.Circ Res1999; 84:973-979.
[8]Geng B,Yang JH,Qi YF,Zhao J,Pang YZ,Du JB,Tang CS.H2S generated by heart in rat and its effects on cardiac function.Biochem Biophys Res Commun 2004; 313:362-368.
[9]Stipanuk MH,Beck PW.Characterization of the enzymic capacity for cysteine desulphydration in liver and kidney of the rat.Biochem J 1982; 206:267-277.
[10]Bukovska G,Kery V,Krous JP.Expression of human cystathionine beta-synthase in Escherichia coli purification and characterization.Protein Expr Purif 1994; 5:442-448.
[11]Swaroop M,Bradley K,Ohura T,Tahara T,Roper MD,Rosenberg LE,Kraus JD.Rat cystathionine β-synthase gene organization and alternative splicing.J Biol them 1992; 267:11455-11461.
[12]Hosoki R,Matsuki N,kimura H.The possible role of hydrogen sulfide as an endogenous smooth muscle relaxant in synergy with nitric oxide.Biochem Biophys Res Commun 1997; 273:527-531.
[13]Zhao WM,Joseph FN,Wang R.Modulation of endogenous production of H2S in rat tissues.Can J Physiol Pharmacol 2003;81:848-853,
[14]Xiao L,Wu YM,Zhang H,Liu YX,He RR.Hydrogen sulfide facilitates carotid sinus baroreflex in anesthetized rats.Acta Pharmacol Sin 2006; 27(3):294-298.
[15]Xu M,Wu YM,Li Q,Wang FW,He RR.Electrophysiological effects of hydrogen sulfide on guinea pig papillary muscles.Acta Physiol Sin (生理学报) 2007; 59(2):215-220.
[16]Zhang Z,Li YL,He RR.Effects of endothelin on the electrical activity of sino-atrial pacemaker cells of rabbits.Acta Physiol Sin (生理学报) 1996; 48(1):53-58.
[17]Fan ZZ,An RH,He RR.System of sampling and processing cardiac transmembrane potential by microcomputer.Chin J Phys Med (中华物理医学杂志) 1991; 13:39-42.
[18]Van Ginneken AC,Giles W.Voltage clamp measurements of the hyperpolarization-activated inward current (If) in single ceilsfrom rabbit sino-atrial node.J Physiol 1991; 434:57-83.
[19]Vassalle M.The pacemaker current (It) does not play an important role in regulating SA node pacemaker activity.Cardiovasc Res1995; 30(2):309-310.
[20]Kakei M,Noma A,Shibasaki T.Properties of adenosinetriphosphate-regulated potassium channels in guinea pig ventrticular cells.J Physiol 1985; 363:441-462.
[21]De WeiUe JR.Modulation of ATP sensitive potassium channels.Cardiovasc Res 1992; 26:1017-1020.
[22]Qin DY,Takano M,Noma A.Kinetics of ATP-sensitive K+ channels revealed with oil-gate concentration jump method.Am J Physiol 1989; 257:H1624-HI633.
[23]Denyer JC,Brown HF.Pacemaking in rabbit isolated sino-atrial node ceils during Cs+ block of the hyperpolarization-activated current If.J Physiol 1990; 429:401-409.
[24]Chen P,Poddar R,Tipa EV,Dibello PM,Moravec CD,Robinson K,Green R,Kruger WD,Garrow TA,Jacobsen DW.Homocysteine metabolism in cardiovascular cells and tissues:implications for hyperhomocysteinemia and cardiovascular disease.Adv Enzyme Regul 1999; 39:93-109.
[25]Bian JS,Yong QC,Pan TT,Feng ZN,Ali MY,Zhou S,Moore PK.Role of hydrogen sulfide in the cardioprotection caused by ischemic preconditioning in the rat heart and cardiac myocytes.J Pharmacol Exper Ther 2006; 316:670-678.