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Research Article

Bronchoconstrictor effect of the tachykinin NK3-receptor agonists [MePhe7]-neurokinin B and senktide in the isolated guinea pig lung

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Pages 509-521 | Received 09 Feb 2010, Accepted 15 Mar 2010, Published online: 13 Oct 2010
 

ABSTRACT

To determine whether bronchoconstriction can be mediated via the tachykinin NK3 receptors, isolated guinea pig lungs were challenged with the exogenous tachykinin NK3-receptor agonists [MePhe7]-neurokinin B ([MePhe7]-NKB) and senktide. [MePhe7]-NKB induced bronchoconstriction (EC50 = 11.8 ± 1.7 μM) that was significantly inhibited by the tachykinin NK3-receptor antagonist SB 223412 at 10 μM (EC50 = 24.4 ± 4.5 μM). Senktide also induced bronchoconstriction (EC50 = 96.2 ± 20.3 μM) and the bronchoconstriction was significantly reduced by SB 223412 at 1 and 10 μM (EC50 = 270.8 ± 78.9 μM and 388.3 ± 105.5 μM, respectively). Although the authors demonstrated that SB 223412, [MePhe7]-NKB, and senktide are potent and selective for the tachykinin NK3 receptors in binding and functional (Ca2+ mobilization) assays, the tachykinin NK1-receptor antagonist CP 99,994 at 1 μM (EC50 = 32.7 ± 8.5 μM) produced inhibition of [MePhe7]-NKB–induced bronchoconstriction, whereas the tachykinin NK2-receptor antagonist SR 48968 at 0.1 μM (EC50 = 213.2 ± 42.9 μM) blocked senktide-induced bronchoconstriction. These data suggest that [MePhe7]-NKB and senktide caused bronchoconstriction in guinea pig through activation of the tachykinin NK3-receptors but the tachykinin NK1- and/or NK2-receptors are also involved in the response.

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