Fukuhara S, Mukai H, Munekata E
Institute of Applied Biochemistry, University of Tsukuba, Ibaraki, Japan.
Peptides. 1995;16(2):211-4. doi: 10.1016/0196-9781(94)00166-9.
We found that neurokinin A (NKA) and neurokinin B (NKB) induce an increase in the concentration of intracellular free Ca2+ ([Ca2+]i) in murine neuroblastoma C1300 cells (EC50: NKA 87 +/- 13 nM, NKB 97 +/- 15 nM). Substance P (SP) also caused a transient Ca2+ increase, although the potency of SP was much less than that of NKA and NKB. The increase in [Ca2+]i induced by NKA and NKB was inhibited by SR 48,968, a selective antagonist for NK2, and [beta Ala8]NKA(4-10), a selective agonist for NK2, did not stimulate the increase in [Ca2+]i. NKA- and NKB-induced Ca2+ mobilization was not inhibited by CP-96,345 and [Trp7, beta Ala8]NKA(4-10), selective antagonists for NK1 and NK3, respectively. These results suggested that C1300 cells express endogenous NK2 neurokinin receptors that have different features from known NK2 receptors.
我们发现，神经激肽A（NKA）和神经激肽B（NKB）可使小鼠神经母细胞瘤C1300细胞内游离Ca2+（[Ca2+]i）浓度升高（半数有效浓度：NKA为87±13 nM，NKB为97±15 nM）。P物质（SP）也可引起Ca2+短暂升高，尽管其效力远低于NKA和NKB。NKA和NKB诱导的[Ca2+]i升高被NK2选择性拮抗剂SR 48,968抑制，而NK2选择性激动剂[β丙氨酸8]NKA(4 - 10)并未刺激[Ca2+]i升高。NKA和NKB诱导的Ca2+动员不受NK1和NK3选择性拮抗剂CP - 96,345和[色氨酸7，β丙氨酸8]NKA(4 - 10)的抑制。这些结果表明，C1300细胞表达内源性NK2神经激肽受体，其具有与已知NK2受体不同的特征。
