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1 Department of Molecular and Cellular Physiology, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0576; and 2 Division of Nephrology, Departments of Medicine and Pharmacology, Vanderbilt University, Nashville, Tennessee 37232-2372
Substance P (SP) and ATP evoke
transient, epithelium-dependent relaxation of constricted mouse
tracheal smooth muscle. Relaxation to either SP or ATP is blocked by
indomethacin, but the specific eicosanoid(s) involved have not been
definitively identified. SP and ATP are reported to release
PGE2 from airway epithelium in other species, suggesting
PGE2 as a likely mediator in epithelium-dependent airway
relaxation. Using mice homozygous for a gene-targeted deletion of the
EP2 receptor [EP2(
/)], one of the
PGE2 receptors, we tested the hypothesis that
PGE2 is the primary mediator of relaxation to SP or ATP.
Relaxation in response to SP or ATP was significantly reduced in
tracheas from EP2(/) mice. There were no differences between EP2(/) and wild-type tracheas in their physical
dimensions, contraction to ACh, or relaxation to isoproterenol, thus
ruling out any general alterations of smooth muscle function. There
were also no differences between EP2(/) and wild-type
tracheas in basal or stimulated PGE2 production. Exogenous
PGE2 produced significantly less relaxation in
EP2(/) tracheas compared with the wild type. Taken
together, this experimental evidence supports the following two
conclusions: EP2 receptors are of primary importance in
airway relaxation to PGE2 and relaxation to SP or ATP is
mediated through PGE2 acting on EP2 receptors.
smooth muscle; airway; adenosine 5'-triphosphate; mice; mouse; prostaglandin E2
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