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1 Pharmacology Group and Vascular Biology Research Centre, School of Biomedical Sciences, King's College, London SW3 6LX, United Kingdom; and 2 The Children's Hospital, Perlmutter Laboratory, Boston, Massachusetts 02115
The mechanisms involved in tachykinin-induced neurokinin-1 (NK1) receptor-mediated edema formation have been studied in anesthetized wild-type and NK1 knockout mice. Intradermally injected substance P (30-300 pmol), NK1 agonists septide (3-30 pmol) and GR-73632 (3-30 pmol), and the mast cell-degranulating agent, compound 48/80 induced dose-dependent edema in wild-type skin, measured by the accumulation of intravenously injected 125I-labeled albumin. Septide was 3-10× more potent than substance P. The tachykinins were inactive in knockout mice, but compound 48/80 induced a significantly greater edema (P < 0.05) than that observed in paired wild-type mice. Capsaicin (which releases endogenous neuropeptides) and exogenous tachykinins induced edema formation, which was reduced by the mast cell amine histamine H1 antagonist mepyramine (P < 0.05). These findings confirm that tachykinins mediate edema formation via the NK1 receptor and provide direct evidence that the septide-sensitive binding site is on the NK1 receptor. Furthermore, results suggest that edema induced by the tachykinins, although totally dependent on NK1 receptor-mediated mechanism, contains a mast cell-dependent component. The evidence is in keeping with an NK1 receptor on mast cells.
neurokinin-1 receptor; substance P; neurokinin-1 knockout mouse; edema formation; rat skin; tachykinins; neurokinins
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