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Am J Physiol Lung Cell Mol Physiol 283: L1151-L1159, 2002. First published June 28, 2002; doi:10.1152/ajplung.00038.2002
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Vol. 283, Issue 5, L1151-L1159, November 2002

Receptors and signaling pathway underlying relaxations to isoprostanes in canine and porcine airway smooth muscle

Adriana Catalli, Dawei Zhang, and Luke J. Janssen

Asthma Research Group, Father Sean O'Sullivan Research Center, Firestone Institute for Respiratory Health, St. Joseph's Hospital; and Department of Medicine, McMaster University, Hamilton, Ontario, Canada L8N 4A6

Using muscle bath techniques, we examined the inhibitory activities of several E- and F-ring isoprostanes in canine and porcine airway smooth muscle. 8-Isoprostaglandin E1 and 8-isoprostaglandin E2 (8-iso PGE2) reversed cholinergic tone in a concentration-dependent manner, whereas the F-ring isoprostanes were ineffective. Desensitization with 8-iso-PGE2 and PGE2 implicated isoprostane activity at the PGE2 receptor (EP). We found that the inhibitory E-ring isoprostane responses were significantly augmented by rolipram (a type IV phosphodiesterase inhibitor), while 1H-[1,2,4]-oxadiazolo[4,3-a]quinoxalin-1-one (a guanylate cyclase inhibitor) had no effect, suggesting a role for cAMP in isoprostane-mediated relaxations. 8-Iso-PGE2 did not reverse KCl tone, suggesting that voltage-dependent Ca2+ influx and myosin light chain kinase are not suppressed by isoprostanes. Patch-clamp studies showed marked suppression of K+ currents by 8-iso-PGE2. We conclude that E-ring isoprostanes exert PGE2 receptor-directed, cAMP-dependent relaxations in canine and porcine airway smooth muscle. This activity is not dependent on K+ channel activation or the direct inhibition of voltage-operated Ca2+ influx or myosin light chain kinase.

cyclic nucleotides; potassium channels; calcium channels; prostanoid receptors


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