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• W2188196729 startingPage "R476" @default.
• W2188196729 abstract "The mechanisms involved in tachykinin-induced neurokinin-1 (NK 1 ) receptor-mediated edema formation have been studied in anesthetized wild-type and NK 1 knockout mice. Intradermally injected substance P (30–300 pmol), NK 1 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 125 I-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 H 1 antagonist mepyramine ( P < 0.05). These findings confirm that tachykinins mediate edema formation via the NK 1 receptor and provide direct evidence that the septide-sensitive binding site is on the NK 1 receptor. Furthermore, results suggest that edema induced by the tachykinins, although totally dependent on NK 1 receptor-mediated mechanism, contains a mast cell-dependent component. The evidence is in keeping with an NK 1 receptor on mast cells." @default.
• W2188196729 created "2016-06-24" @default.
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• W2188196729 date "1999-08-01" @default.
• W2188196729 modified "2023-10-17" @default.
• W2188196729 title "Use of NK₁knockout mice to analyze substance P-induced edema formation" @default.
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• W2188196729 doi "https://doi.org/10.1152/ajpregu.1999.277.2.r476" @default.
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