title: [Adenosine reduces intracellular free calcium concentration in guinea pig ventricular myocytes].
abstract: OBJECTIVE
  To observe the effects of adenosine on intracellular calcium concentration ([Ca2+]i) level in guinea pig ventricular myocytes and to define the possible mechanisms involved.
  
  
  METHODS
  The effects of adenosine on [Ca2+]i were investigated in guinea pig ventricular myocytes. [Ca2+]i was detected by laser confocal microscopy and represented by relative fluorescent intensity ((FI-FI0)/FI0, %, FIo: control, FI: administration of drugs).
  
  
  RESULTS
  (1) Adenosine (10, 50, 100 micromol/L) reduced [Ca2+]i of ventricular myocytes in both normal Tyrode's solution and Ca(2+) -free Tyrode's solution in a concentration-dependent manner. (2) Tyrode's solution containing 30 mmol/L KCl (high K+ Tyrode's solution) induced [Ca2+]i elevation in ventricular myocytes, while adenosine (10, 50, 100 micromol/L) markedly inhibited the increase in [Ca2+]i induced by KCl. (3) Pretreatment with DPCPX (1 micromol/L) significantly reduced the effects of adenosine (100 micromol/L) in high K+ Tyrode's solution. The effects of adenosine (100 micromol/L) on [Ca2+]i in high K+ Tyrode's solution were also partially attenuated by pretreatment with L-NAME (1 mmol/L). (4) Adenosine (100 micromol/L) markedly inhibited the low concentration of ryanodine-induced [Ca2+]i increase in Ca(2+) -free Tyrode's solution. (5) When the propagating waves of elevated [Ca2+]i (Ca2+ waves) were produced by increasing extracellular Ca2+ concentration from 1 mmol/L to 10 mmol/L, adenosine (100 micromol/L) could block the propagating waves of elevated [Ca2+]i, reduce the frequency and duration of propagating waves, and reduce [Ca2+]i as well.
  
  
  CONCLUSIONS
  Adenosine may reduce the [Ca2+]i in isolated guinea pig ventricular myocytes via inhibiting Ca2+ influx and alleviating Ca2+ release from sarcoplasmic reticulum(SR). The reduction of Ca2+ influx might be due to the inhibition of voltage-dependent Ca2+ channel via adenosine A1 receptor, and NO might be involved in this process.
authors.affiliation: Department of Physiology, Hebei Medical University, Shijiazhuang 050017, China.
authors.forename: Hui-Jie
authors.initials: HJ
authors.lastname: Ma
authors.forename: Mei
authors.initials: M
authors.lastname: Dong
authors.forename: En-Sheng
authors.initials: ES
authors.lastname: Ji
authors.forename: Chuan
authors.initials: C
authors.lastname: Wang
authors.forename: Jing-Xiang
authors.initials: JX
authors.lastname: Yin
authors.forename: Qing-Shan
authors.initials: QS
authors.lastname: Wang
mesh_terms: D000241:Adenosine / Q000494:pharmacology*; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002478:Cells, Cultured; D006168:Guinea Pigs; D006352:Heart Ventricles / Q000166:cytology; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism*
chemical_list: D000241:Adenosine; D002118:Calcium