Endogenous adenosine and ATP-sensitive potassium channel modulate anoxia-induced electrophysiological changes of pacemaker cells in sinoatrial node of guinea pigs

Y. L. Li, R. R. He

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Aim: To investigate the electrophysiological effects of adenosine deaminase (ADase, an enzyme converting adenosine to inosine and ammonia), 8-phenyltheophylline (8-PT, a nonselective antagonist of adenosine receptors) and glibenclamide (Gli, a potent blocker of ATP-sensitive K+ channels) on anoxic pacemaker cells of SA node. Methods: Anoxia of pacemaker cells in SA node of guinea-pig was induced by perfused for 20 min with a modified K-H solution gassed with 100 % N2 deprived of glucose. Parameters of action potentials including maximal diastolic potential (MDP), amplitude of action potential (APA), duration of 90 % repolarization (APD90), maximal rate of depolarization (V(max)), rate of pacemaker firing (RPF), and velocity of diastolic (phase 4) depolarization (VDD) were recorded using intracellular microelectrodes. Results: Anoxia increased MDP, APA, and V(max) and decreased VDD, RPF in a time-dependent manner. ADase 10 U · L-1, 8-PT 0.1 μmol · L-1 and Gli 10 μmol · L-1 significantly attenuated the electrophysiological changes of pacemaker cells in sinoatrial node induced by anoxia. Conclusion: Endogenous adenosine and ATP-sensitive K+ channels may play an important role in the generation of anoxic bradycardia in guinea pigs.

Original languageEnglish (US)
Pages (from-to)42-46
Number of pages5
JournalActa Pharmacologica Sinica
Volume16
Issue number1
StatePublished - Jan 16 1995

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Pacemakers
KATP Channels
Sinoatrial Node
Adenosine
Action Potentials
Guinea Pigs
Adenosine Triphosphate
Purinergic P1 Receptor Antagonists
Depolarization
Cell Hypoxia
Inosine
Adenosine Deaminase
Glyburide
Microelectrodes
Bradycardia
Ammonia
Glucose
Enzymes
Hypoxia

Keywords

  • adenosine
  • adenosine deaminase
  • anoxia
  • electrophysiology
  • glyburide
  • potassium channels
  • sinoatrial node

ASJC Scopus subject areas

  • Pharmacology
  • Pharmacology (medical)

Cite this

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title = "Endogenous adenosine and ATP-sensitive potassium channel modulate anoxia-induced electrophysiological changes of pacemaker cells in sinoatrial node of guinea pigs",
abstract = "Aim: To investigate the electrophysiological effects of adenosine deaminase (ADase, an enzyme converting adenosine to inosine and ammonia), 8-phenyltheophylline (8-PT, a nonselective antagonist of adenosine receptors) and glibenclamide (Gli, a potent blocker of ATP-sensitive K+ channels) on anoxic pacemaker cells of SA node. Methods: Anoxia of pacemaker cells in SA node of guinea-pig was induced by perfused for 20 min with a modified K-H solution gassed with 100 {\%} N2 deprived of glucose. Parameters of action potentials including maximal diastolic potential (MDP), amplitude of action potential (APA), duration of 90 {\%} repolarization (APD90), maximal rate of depolarization (V(max)), rate of pacemaker firing (RPF), and velocity of diastolic (phase 4) depolarization (VDD) were recorded using intracellular microelectrodes. Results: Anoxia increased MDP, APA, and V(max) and decreased VDD, RPF in a time-dependent manner. ADase 10 U · L-1, 8-PT 0.1 μmol · L-1 and Gli 10 μmol · L-1 significantly attenuated the electrophysiological changes of pacemaker cells in sinoatrial node induced by anoxia. Conclusion: Endogenous adenosine and ATP-sensitive K+ channels may play an important role in the generation of anoxic bradycardia in guinea pigs.",
keywords = "adenosine, adenosine deaminase, anoxia, electrophysiology, glyburide, potassium channels, sinoatrial node",
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AU - Li, Y. L.

AU - He, R. R.

PY - 1995/1/16

Y1 - 1995/1/16

N2 - Aim: To investigate the electrophysiological effects of adenosine deaminase (ADase, an enzyme converting adenosine to inosine and ammonia), 8-phenyltheophylline (8-PT, a nonselective antagonist of adenosine receptors) and glibenclamide (Gli, a potent blocker of ATP-sensitive K+ channels) on anoxic pacemaker cells of SA node. Methods: Anoxia of pacemaker cells in SA node of guinea-pig was induced by perfused for 20 min with a modified K-H solution gassed with 100 % N2 deprived of glucose. Parameters of action potentials including maximal diastolic potential (MDP), amplitude of action potential (APA), duration of 90 % repolarization (APD90), maximal rate of depolarization (V(max)), rate of pacemaker firing (RPF), and velocity of diastolic (phase 4) depolarization (VDD) were recorded using intracellular microelectrodes. Results: Anoxia increased MDP, APA, and V(max) and decreased VDD, RPF in a time-dependent manner. ADase 10 U · L-1, 8-PT 0.1 μmol · L-1 and Gli 10 μmol · L-1 significantly attenuated the electrophysiological changes of pacemaker cells in sinoatrial node induced by anoxia. Conclusion: Endogenous adenosine and ATP-sensitive K+ channels may play an important role in the generation of anoxic bradycardia in guinea pigs.

AB - Aim: To investigate the electrophysiological effects of adenosine deaminase (ADase, an enzyme converting adenosine to inosine and ammonia), 8-phenyltheophylline (8-PT, a nonselective antagonist of adenosine receptors) and glibenclamide (Gli, a potent blocker of ATP-sensitive K+ channels) on anoxic pacemaker cells of SA node. Methods: Anoxia of pacemaker cells in SA node of guinea-pig was induced by perfused for 20 min with a modified K-H solution gassed with 100 % N2 deprived of glucose. Parameters of action potentials including maximal diastolic potential (MDP), amplitude of action potential (APA), duration of 90 % repolarization (APD90), maximal rate of depolarization (V(max)), rate of pacemaker firing (RPF), and velocity of diastolic (phase 4) depolarization (VDD) were recorded using intracellular microelectrodes. Results: Anoxia increased MDP, APA, and V(max) and decreased VDD, RPF in a time-dependent manner. ADase 10 U · L-1, 8-PT 0.1 μmol · L-1 and Gli 10 μmol · L-1 significantly attenuated the electrophysiological changes of pacemaker cells in sinoatrial node induced by anoxia. Conclusion: Endogenous adenosine and ATP-sensitive K+ channels may play an important role in the generation of anoxic bradycardia in guinea pigs.

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