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1 Le Bilarium, Department of Physiology and Biophys, University of Sherbrooke, Sherbrooke, QC, Canada
2 Claude Pepper Institute and Department of Chemistry, Florida Institute of Technology, Melbourne, Fl, USA
3 Meakins-Christie Lab., McGill University, Montreal, QC, Canada
* To whom correspondence should be addressed. E-mail: eric.rousseau{at}usherbrooke.ca.
5-Oxo-6,8,11,14-eicosatetraenoic (5-oxo-ETE) is a pro-inflammatory mediator but its effects on airway smooth muscle (ASM) have never been assessed. Tension measurements performed on guinea pig ASM showed that 5-oxo-ETE induced sustained concentration-dependant positive inotropic responses (EC50 = 0.89 µM) of somewhat lower amplitude than those induced by carbamylcholine and the thromboxane A2 (TXA2) agonist U-46619. Transient inotropic responses to 5-oxo-ETE were recorded in Ca2+ free medium, suggesting mobilization of intracellular Ca2+. Meanwhile, the sustained contraction, which required Ca2+ entry, was partially blocked by 1 µM nifedipine (an Ltype Ca2+ channel blocker) but relatively insensitive to 100 µM Gd3+. The 5-oxo-ETE responses were also inhibited by indomethacin and SC560 (a COX-1 inhibitor) pretreatments but not by NS-398, (a selective COX-2 inhibitor). The contractile effects of 5-oxo-ETE on ASM were inhibited by the selective TP receptor antagonist SQ 29,548 (- 75%) and by ONO-RS-082 pre-treatment, a PLA2 inhibitor(-66 %), suggesting that the major part of its effect is mediated by the release of TXA2. ASM responses to 5-oxo-ETE were also blocked by the Rho-kinase inhibitor, Y-27632, which also partially inhibited the response to the TP receptor agonist U-46619, suggesting that the contractile response is due in part to Ca2+ sensitization of ASM cell myofilaments.
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