ATP release by cardiac myocytes in a simulated ischaemia model: inhibition by a connexin mimetic and enhancement by an antiarrhythmic peptide

Thomas C. Clarke, Oliver J.S. Wlliams, Patricia E.M. Martin, W. Howard Evans

Research output: Contribution to journalArticle

Abstract

We studied the role of connexin hemichannels in the release of ATP by neonatal cardiac myocytes subject to ischaemic stress. Mechanical, osmotic and oxidative stress and changes in extracellular or intracellular Ca2+ levels induce connexin hemichannels located in the plasma membrane to open and release small ions and molecules with signaling potential such as ATP. Since ATP release has been implicated in adaptation to oxygen deprivation, we studied its release by cardiac myocytes incubated in a custom-built hypoxia chamber for various periods. In a simulated ischaemia model (0.5% oxygen and 0.2 g/l glucose) a peak of ATP release occurred at 80 min followed by a return to steady state levels for a further 200 min.

Original languageEnglish
Pages (from-to)9-14
Number of pages6
JournalEuropean Journal of Pharmacology
Volume605
Issue number1-3
DOIs
Publication statusPublished - 1 Mar 2009

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Connexins
Cardiac Myocytes
Ischemia
Adenosine Triphosphate
Oxygen
Mechanical Stress
Osmotic Pressure
Oxidative Stress
Cell Membrane
Ions
Glucose
antiarrhythmic peptide

Keywords

  • connexins
  • ischaemic stress
  • ATP

Cite this

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title = "ATP release by cardiac myocytes in a simulated ischaemia model: inhibition by a connexin mimetic and enhancement by an antiarrhythmic peptide",
abstract = "We studied the role of connexin hemichannels in the release of ATP by neonatal cardiac myocytes subject to ischaemic stress. Mechanical, osmotic and oxidative stress and changes in extracellular or intracellular Ca2+ levels induce connexin hemichannels located in the plasma membrane to open and release small ions and molecules with signaling potential such as ATP. Since ATP release has been implicated in adaptation to oxygen deprivation, we studied its release by cardiac myocytes incubated in a custom-built hypoxia chamber for various periods. In a simulated ischaemia model (0.5{\%} oxygen and 0.2 g/l glucose) a peak of ATP release occurred at 80 min followed by a return to steady state levels for a further 200 min.",
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ATP release by cardiac myocytes in a simulated ischaemia model: inhibition by a connexin mimetic and enhancement by an antiarrhythmic peptide. / Clarke, Thomas C.; Wlliams, Oliver J.S.; Martin, Patricia E.M.; Evans, W. Howard.

In: European Journal of Pharmacology, Vol. 605, No. 1-3, 01.03.2009, p. 9-14.

Research output: Contribution to journalArticle

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AU - Clarke, Thomas C.

AU - Wlliams, Oliver J.S.

AU - Martin, Patricia E.M.

AU - Evans, W. Howard

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