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P物质诱导的大鼠皮肤血浆外渗由NK-1速激肽受体介导。

Substance P-induced cutaneous plasma extravasation in rats is mediated by NK-1 tachykinin receptors.

作者信息

Devor M, Papir-Kricheli D, Nachmias E, Rosenthal F, Gilon C, Chorev M, Selinger Z

机构信息

Department of Zoology, Hebrew University of Jerusalem, Israel.

出版信息

Neurosci Lett. 1989 Aug 28;103(2):203-8. doi: 10.1016/0304-3940(89)90576-4.

DOI:10.1016/0304-3940(89)90576-4
PMID:2475833
Abstract

Substance P (SP), a relatively non-selective tachykinin receptor agonist, and Septide and Senktide, highly selective NK-1 and NK-3 tachykinin receptor agonists, respectively, were injected intradermally in rats. The resulting cutaneous plasma extravasation (PE) was evaluated by measuring the amount of Evans blue that leached from the circulation into the skin. SP and Septide produced dose dependent PE, Septide being the more potent of the two. Senktide did not produce PE, even at doses 10,000 times higher. Neonatal capsaicin treatment significantly reduced SP- and Septide-induced PE. These data indicate that SP-induced PE is mediated by NK-1 tachykinin receptors.

摘要

P物质(SP)是一种相对非选择性的速激肽受体激动剂,而Septide和Senktide分别是高度选择性的NK-1和NK-3速激肽受体激动剂,将它们皮内注射到大鼠体内。通过测量从循环中渗入皮肤的伊文思蓝的量来评估由此产生的皮肤血浆外渗(PE)。SP和Septide产生剂量依赖性的PE,其中Septide的作用更强。即使剂量比前者高10000倍,Senktide也不会产生PE。新生大鼠用辣椒素处理可显著降低SP和Septide诱导的PE。这些数据表明,SP诱导的PE是由NK-1速激肽受体介导的。

相似文献

1
Substance P-induced cutaneous plasma extravasation in rats is mediated by NK-1 tachykinin receptors.P物质诱导的大鼠皮肤血浆外渗由NK-1速激肽受体介导。
Neurosci Lett. 1989 Aug 28;103(2):203-8. doi: 10.1016/0304-3940(89)90576-4.
2
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Br J Pharmacol. 1992 Aug;106(4):888-92. doi: 10.1111/j.1476-5381.1992.tb14430.x.

引用本文的文献

1
Characterization of central and peripheral effects of septide with the use of five tachykinin NK1 receptor antagonists in the rat.利用五种速激肽NK1受体拮抗剂对大鼠进行研究以表征septide的中枢和外周效应
Br J Pharmacol. 1999 Jun;127(3):717-28. doi: 10.1038/sj.bjp.0702620.
2
Demonstration of a 'septide-sensitive' inflammatory response in rat skin.大鼠皮肤中“septide敏感”炎症反应的证明。
Br J Pharmacol. 1995 Oct;116(4):2170-4. doi: 10.1111/j.1476-5381.1995.tb15050.x.