Adenosine attenuates calcium paradox injury: Role of adenosine A1 receptor

J. Suleiman, Muhammad Ashraf

Research output: Contribution to journalArticle

13 Scopus citations

Abstract

The present study was conducted to test the hypothesis that adenosine attenuates the Ca2+ paradox (PD) injury via stimulation of adenosine A1 receptors linked to G(i) proteins in the isolated rat heart. Treatment of adenosine reduced maximum lactate dehydrogenase release and ATP loss compared with regular Ca2+ PD. Recovery of mechanical activity after Ca2+ repletion was observed only in heart treated with adenosine before and during the Ca2+ PD. Significant preservation of myocytes was observed in adenosine-treated hearts compared with the regular Ca2+ PD. Adenosine exerted its effects in a dose-dependent manner, being maximum at 100 μM. The protective effects were mediated by adenosine A1 receptor activation since the adenosine A1 receptor agonist N6-phenylisopropyladenosine provided protection similar to adenosine-treated heart and was blocked by A1 receptor antagonist and pertussis toxin. This study suggests that protection by adenosine against the lethal injury of the Ca2+ PD is mediated by adenosine A1 receptor and a pertussis toxin-sensitive inhibiting G protein.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Cell Physiology
Volume268
Issue number4 37-4
StatePublished - May 9 1995
Externally publishedYes

Keywords

  • G protein
  • pertussis toxin

ASJC Scopus subject areas

  • Physiology
  • Cell Biology

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