Effects of arachidonic acid on the gap junctions of neonatal rat heart cells

1990 ◽  
Vol 417 (2) ◽  
pp. 149-156 ◽  
Author(s):  
Gisela Schmilinsky Fluri ◽  
Anton R�dis�li ◽  
Marius Willi ◽  
Stephan Rohr ◽  
Robert Weingart
Keyword(s):  
Arachidonic Acid ◽  
Gap Junctions ◽  
Rat Heart ◽  
Neonatal Rat ◽  
Heart Cells ◽  
Neonatal Rat Heart ◽  
Rat Heart Cells

Chronotropic effect of histamine on cultured neonatal rat heart cells

1979 ◽  
Vol 58 (2) ◽  
pp. 117-123 ◽  
Author(s):  
Klara Csete ◽  
Marie-Claude Auclair ◽  
Paul Lechat
Keyword(s):  
Rat Heart ◽  
Neonatal Rat ◽  
Heart Cells ◽  
Chronotropic Effect ◽  
Neonatal Rat Heart ◽  
Rat Heart Cells

Arachidonic acid and lipoxygenase metabolites uncouple neonatal rat cardiac myocyte pairs

1992 ◽  
Vol 263 (2) ◽  
pp. C494-C501 ◽  
Author(s):  
K. D. Massey ◽  
B. N. Minnich ◽  
J. M. Burt
Keyword(s):  
Arachidonic Acid ◽  
Gap Junctions ◽  
Cardiac Myocyte ◽  
Underlying Mechanism ◽  
Neonatal Rat ◽  
Heart Cells ◽  
Membrane Phospholipids ◽  
Lipoxygenase Pathway ◽  
Rat Heart Cells ◽  
The Right

The effects of arachidonic acid (AA) and its metabolites on the conductance (gj) of the gap junctions between neonatal rat myocardial cells was investigated. AA reduced gj in a dose- (2, 5, and 20 microM) 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 less than 0.05) for 5 microM AA, 5 microM AA + indomethacin, and 5 microM 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.

Sign in / Sign up

Export Citation Format

Share Document