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The actions of arachidonic acid (AA) were investigated in guinea-pig isolated ventricular myocytes. Exposure of myocytes to 10 microM AA reduced the amplitude of contractions and calcium transients accompanying action potentials at a frequency of 1 Hz. AA (10 microM) also reduced the amplitude of calcium currents recorded under voltage-clamp conditions. The suppression of contraction by AA was not prevented by either 10 microM trihydroindomethicin (to inhibit cyclo-oxygenase) or 10 microM ETYA (5,8,11,14-eicosatetraynoic acid, to inhibit AA metabolising enzymes), showing that the actions of AA appeared not to be mediated by these metabolites. The reduction of contraction by 10 microM AA was also not prevented by the protein kinase C inhibitor, Ro31-8220 (1 microM), showing that this pathway appeared not to be required for the observed effect. Direct effects of AA may be involved. A further action of 10 microM AA was to suppress spontaneous electrical activity induced by either the beta-adrenergic agonist isoprenaline or the Na(+) pump inhibitor, ouabain. This effect of AA on spontaneous activity might be associated with the observed reduction of calcium entry through L-type calcium channels, although additional effects of AA on calcium release from the sarcoplasmic reticulum might also be involved. Experimental Physiology (2001) 86.4, 437-449.

Type

Journal article

Journal

Exp Physiol

Publication Date

07/2001

Volume

86

Pages

437 - 449

Keywords

5,8,11,14-Eicosatetraynoic Acid, 8-Bromo Cyclic Adenosine Monophosphate, Action Potentials, Animals, Arachidonic Acid, Calcium, Calcium Channels, L-Type, Cardiotonic Agents, Cyclooxygenase Inhibitors, Delayed Rectifier Potassium Channels, Enzyme Inhibitors, Guinea Pigs, Heart Ventricles, In Vitro Techniques, Indoles, Indomethacin, Isoproterenol, Muscle Fibers, Skeletal, Myocardial Contraction, Myocardium, Ouabain, Patch-Clamp Techniques, Potassium Channels, Potassium Channels, Voltage-Gated, Protein Kinase C