NK1 receptors mediate tachykinin-induced plasma extravasation in the rat knee joint

Publisher Website
Google Scholar
Abstract
The tachykinin receptor type that medicates tachykinin-induced plasma extravasation in the rat knee joint was identified by using selective antagonists as well as natural or synthetic agonists. Substance P (SP) and neurokinin (NK) A induced plasma extravasation with almost the same potency and the maximum response was obtained at 5 nmol/knee. NKB was about ten times less potent than SP or NKA. The NK1 selective agonist, [Sar9, Met(O2)11]-SP, was about ten times more potent than SP, and the NK2 selective agonist, [Nle10]-NKA4–10, was about fifty times less potent than NK1 agonist. The NK3 agonist, Senktide, was totally ineffective at 0.5–50 nmol/knee. All responses induced by SP (5 nmol/knee), NKA (5 nmol/knee), NKB (50 nmol/knee), NK1 agonsit (0.5 nmol/knee) or NK2 agonist (25 nmol/knee) were significantly and profoundly inhibited by the NK1 selective antagonist, RP67580, but not by the NK2 selective antagonist, SR48968. Taken together, we conclude that tachykinin-induced plasma extravasation in the rat knee joint is mediated via NK1 receptors.