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Receptor subtypes involved in tachykinin-mediated edema formation

, : Receptor subtypes involved in tachykinin-mediated edema formation. Peptides (New York) 20(8): 921-927

Intradermal (ID) injection of the natural tachykinins substance P (SP), neurokinin A (NKA), and neurokinin B (NKB) (0.3-30 nmol) resulted in a marked and dose-related rat paw edema, with mean ED50 values of 2.68 nmol, 1.17 nmol, and 0.80 nmol, respectively. The ID injection of the selective NK1, SP methyl-ester (1-30 nmol), NK2, (beta-Ala8)-neurokinin A4-10 (beta-Ala, 0.3-30 nmol), or NK3, senktide (1-10 nmol) agonists, caused extensive edema formation with mean ED50S of 0.48 nmol, 0.41 nmol, and 0.18 nmol, respectively. The ID injection of the selective NK1 antagonist FK888 (0.1-3 nmol) produced marked inhibition (94%, 52%, and 66%, respectively) of rat paw edema induced by SP, NKA, or SP methyl-ester. The ID co-injection of the NK2 receptor antagonist SR 48968 elicited a graded inhibition (52%, 67%, and 35%, respectively) of rat paw edema induced by NKA, beta-Ala and, to a lesser extent, the edema caused by SP. Finally, the ID co-injection of the NK3 receptor antagonist SR 142801 significantly inhibited (53%, 76%, 53%, and 100%, respectively) the edema formation caused by NKB and NKA or by SP and senktide. Together, the data of the present study suggest that tachykinin-mediated rat paw edema depends on the activation of NKi, NK2 and NK3 receptor subtypes, with apparent major involvement of NK1 receptors subtypes.


PMID: 10503769

DOI: 10.1016/s0196-9781(99)00082-0

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