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毒蕈碱型乙酰胆碱受体与速激肽NK-2受体在肠道蠕动中的协同作用。

Synergistic role of muscarinic acetylcholine and tachykinin NK-2 receptors in intestinal peristalsis.

作者信息

Holzer P, Maggi C A

机构信息

University Department of Pharmacology, Graz, Austria.

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 1994 Feb;349(2):194-201. doi: 10.1007/BF00169837.

Abstract

It is known that tachykinins (substance P, neurokinin A) participate in the excitatory neural pathways subserving peristaltic motor activity in the intestine. The aim of the present study was to elucidate the types of tachykinin receptor (NK-1 or NK-2) involved in peristalsis by the use of receptor subtype-selective antagonists. Peristaltic motility in isolated segments of the guinea-pig ileum was induced by pumping fluid into the oral end of the intestinal segment. By way of the intraluminal pressure the compliance of the intestinal wall during the preparatory phase and the pressure threshold to trigger the emptying phase of peristalsis were recorded. The tachykinin antagonists were used at concentrations that were at least 30 times in excess of the equilibrium dissociation constants which had previously been evaluated with receptor subtype-selective agonists on the guinea-pig ileum circular muscle. The NK-1 selective antagonist CP-96,345 (0.3 microM) had a slight stimulant influence on peristalsis, whereas the NK-2 selective antagonists MEN-10,376 (10 microM), GR-94,800 (0.3 microM) and SR-48,968 (0.1 microM) led to a small inhibition of motor activity. However, when given after exposure of the ileum to a threshold concentration of atropine (5-20 nM) causing little depression of peristalsis, the tachykinin NK-2 receptor antagonists invariably abolished peristalsis. This synergistic interaction was not seen when SR-48,968 was administered after the ileal segments had been exposed to concentrations of hexamethonium, isoproterenol or calcitonin gene-related peptide that by themselves caused a slight inhibition of peristalsis only.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

已知速激肽(P物质、神经激肽A)参与肠道蠕动性运动活动的兴奋性神经通路。本研究的目的是通过使用受体亚型选择性拮抗剂来阐明参与蠕动的速激肽受体类型(NK-1或NK-2)。通过向豚鼠回肠孤立节段的口端泵入液体来诱导蠕动性运动。通过腔内压力记录准备阶段肠壁的顺应性以及触发蠕动排空阶段的压力阈值。速激肽拮抗剂的使用浓度至少是先前用受体亚型选择性激动剂在豚鼠回肠环行肌上评估的平衡解离常数的30倍以上。NK-1选择性拮抗剂CP-96,345(0.3微摩尔)对蠕动有轻微的刺激作用,而NK-2选择性拮抗剂MEN-10,376(10微摩尔)、GR-94,800(0.3微摩尔)和SR-48,968(0.1微摩尔)导致运动活性略有抑制。然而,当回肠暴露于引起蠕动轻微抑制的阈浓度阿托品(5 - 20纳摩尔)后给予速激肽NK-2受体拮抗剂时,它们总是会消除蠕动。当回肠节段暴露于六甲铵、异丙肾上腺素或降钙素基因相关肽浓度后给予SR-48,968时,未观察到这种协同相互作用,这些物质本身仅引起蠕动的轻微抑制。(摘要截短于250字)

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