A novel motility effect of tachykinins in normal and inflamed colon.

A novel motility effect of tachykinins in normal and inflamed colon.
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速激肽在正常和发炎结肠中的新动力作用。

DOI:
10.1152/ajpgi.1997.272.6.g1607
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发表时间:
1997
期刊:
The American journal of physiology.
影响因子:
--
通讯作者:
Condon,RE
Condon,RE
中科院分区:
--
文献类型:
--
作者:
Tsukamoto,M;Sarna,SK;Condon,RE

文献摘要

被引文献

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通过紧密动脉内输注测试物质,研究了速激肽在刺激清醒狗正常和发炎结肠中的阶段性和巨大迁移性收缩(GMC)中的作用。在低剂量 (0.1 nmol) 下,P 物质和神经激肽 (NK1) 受体激动剂([Sar9,Met(O2)11]P 物质)仅刺激阶段性收缩。在较高剂量 (2.0 nmol) 下,它们刺激阶段性收缩和 GMC。阶段性收缩被先前近距离动脉内输注河豚毒素和阿托品部分但显着地阻断。 NK1 受体拮抗剂不能部分但显着抑制对 P 物质的阶段性收缩反应,而 NK2 和 NK3 受体拮抗剂对 NK2 受体激动剂的收缩反应不到对 P 物质的反应的一半;NK3 受体激动剂不会刺激任何收缩活动。或 NK1、NK2 和 NK3 受体拮抗剂,对 P 物质的收缩反应也不会被 H1 和 H2 受体拮抗剂阻断。炎症抑制了阶段性收缩反应,但增强了 P 物质对 GMC 的刺激。P 物质刺激 GMC 的能力是新颖的,表明其在增加结肠炎症期间这些收缩频率方面的潜在作用。
The role of tachykinins in stimulating phasic and giant migrating contractions (GMCs) in the normal and inflamed colon in conscious dogs was investigated by close-intra-arterial infusions of test substances. At low doses (0.1 nmol), substance P and neurokinin (NK1) receptor agonist ([Sar9,Met(O2)11]substance P] stimulated phasic contractions only. At higher doses (2.0 nmol), they stimulated phasic contractions and GMCs. The phasic contractions were blocked partially but significantly by prior close-intra-arterial infusions of tetrodotoxin and atropine but not by hexamethonium. NK1 receptor antagonist partially but significantly inhibited the phasic contractile response to substance P, whereas NK2 and NK3 receptor antagonists had no significant effect. The contractile response to NK2 receptor agonist was less than one-half of the response to substance P; NK3 receptor agonist did not stimulate any contractile activity. The stimulation of GMCs by higher doses of substance P was not blocked by prior infusions of atropine, tetrodotoxin, or NK1, NK2, and NK3 receptor antagonists, nor was the contractile response to substance P blocked by H1 and H2 receptor antagonists. Inflammation depressed the phasic contractile response but enhanced the stimulation of GMCs by substance P. The ability of substance P to stimulate GMCs is novel and suggests its potential role in increasing the frequency of these contractions during colonic inflammation.