Arachidonic acid and lipoxygenase metabolites uncouple neonatal rat cardiac myocyte pairs

K. D. Massey, B. N. Minnich, Janis M Burt

Research output: Contribution to journalArticle

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Abstract

The effects of arachidonic acid (AA) and its metabolites on the conductance (g(j)) of the gap junctions between neonatal rat myocardial cells was investigated. AA reduced g(j) in a dose- (2, 5, and 20 μM) and time- dependent fashion. Pretreatment of the cells with an inhibitor of the 5- lipoxygenase pathway, U-70344A, shifted the dose-response curve to the right; pretreatment with indomethacin, an inhibitor of the cyclooxygenase pathway, had no effect. The mean time to uncoupling was 3.7 ± 0.3, 3.8 ± 0.9, and 4.6 ± 0.6 min (means ± SE, P < 0.05) for 5 μM AA, 5 μM AA + indomethacin, and 5 μM AA + U-70344A, respectively. Incorporation of AA into membrane phospholipids was not affected by the inhibitor. These studies suggest that complete uncoupling of the cells occurred at membrane concentrations of 3-4 mol%. The data indicate that AA and a 5-lipoxygenase metabolite uncouple neonatal rat heart cells. The data are discussed with respect to the possible underlying mechanism of uncoupling and the potential role of gap junctions in arrhythmia formation in ischemic heart disease.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Cell Physiology
Volume263
Issue number2 32-2
StatePublished - 1992

Fingerprint

Arachidonate Lipoxygenases
Metabolites
Cardiac Myocytes
Arachidonic Acid
Rats
Gap Junctions
Indomethacin
Arachidonate 5-Lipoxygenase
Lipoxygenase Inhibitors
Membranes
Cyclooxygenase Inhibitors
Myocardial Ischemia
Cardiac Arrhythmias
Phospholipids
Cells

Keywords

  • arrhythmia
  • gap junctions
  • heart
  • intercellular communication

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Cell Biology
  • Physiology

Cite this

Arachidonic acid and lipoxygenase metabolites uncouple neonatal rat cardiac myocyte pairs. / Massey, K. D.; Minnich, B. N.; Burt, Janis M.

In: American Journal of Physiology - Cell Physiology, Vol. 263, No. 2 32-2, 1992.

Research output: Contribution to journalArticle

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