1 The aim of the present study was to examine the role of NK1 and NK2 receptors in the control ofmechanical activity of mouse stomach. In this view, the motor effects induced by NK1 and NK2receptor agonists and antagonists were analyzed, measuring motility as intraluminal pressure changesin mouse-isolated stomach preparations. In parallel, immunohistochemical studies were performed toidentify the location of NK1 and NK2 receptors on myenteric neurons and smooth muscle cells.2 Substance P (SP) induced biphasic effects: a contraction followed by relaxation; neurokinin A(NKA) and [b-Ala8]-NKA(410), selective agonist of NK2 receptors, evoked concentrationdependentcontractions, whereas [Sar9, Met(O2)11]-SP, selective agonist of NK1 receptors, inducedconcentration-dependent relaxation.3 SR48968, NK2 receptor antagonist, did not modify the spontaneous activity and reduced thecontractile effects induced by tachykinins without affecting the relaxation. SR140333, NK1 receptorantagonist, did not modify the spontaneous activity and antagonized the relaxant response totachykinins, failing to affect the contractile effects.4 The relaxation to SP or to [Sar9, Met(O2)11]-SP was abolished by tetrodotoxin (TTX) andsignificantly reduced by No-nitro-L-arginine methyl ester (L-NAME).5 NK2-immunoreactivity (NK2-IR) was seen at the level of the smooth muscle cells of both circularand longitudinal muscle layers. NK1-immunoreactive (NK1-IR) neurons were seen in the myentericganglia and NK1/nNOS double labeling revealed that some neurons were both NK1-IR and nNOSIR.6 These results suggest that, in mouse stomach, NK1 receptors, causing relaxant responses, arepresent on nitrergic inhibitory myenteric neurons, whereas NK2 receptors, mediating contractileresponses, are present at muscular level.
|Numero di pagine||7|
|Rivista||British Journal of Pharmacology|
|Stato di pubblicazione||Published - 2006|
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