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Am J Physiol Lung Cell Mol Physiol (June 28, 2002). doi:10.1152/ajplung.00038.2002
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Articles in PresS, published online ahead of print June 27, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00038.2002
Submitted on January 24, 2002
Accepted on June 13, 2002

Receptors and Signaling Pathway Underlying Relaxations to Isoprostanes in Canine and Porcine Airway Smooth Muscle

ADRIANA CATALLI1, DAWEI ZHANG1, and LUKE J JANSSEN1*

1 Department of Medicine, McMaster University, Hamilton, On, Canada

* To whom correspondence should be addressed. E-mail: janssenl{at}mcmaster.ca.

We examined the inhibitory activities of several E-ring and F-ring isoprostanes in canine and porcine airway smooth muscle (ASM) using muscle bath techniques. 8-iso PGE1 and 8-iso PGE2 reversed cholinergic tone in a concentration-dependent manner, while the F-ring isoprostanes were ineffective. Desensitization with 8-iso PGE2 and PGE2 implicated isoprostane activity at the prostanoid EP receptor. We found that the inhibitory E-ring isoprostane responses were significantly augmented by rolipram (PDE IV inhibitor), while ODQ (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 (MLCK) 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 EP receptor-directed, cAMP-dependent relaxations in canine and porcine ASM. This activity is not dependent on K+ channel activation nor the direct inhibition of voltage operated Ca2+ influx or MLCK.




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