Functional difference between SP and NKA: relaxation of gastric muscle by SP is mediated by VIP and NO.
Functional difference between SP and NKA: relaxation of gastric muscle by SP is mediated by VIP and NO.
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SP和NKA之间的功能差异：SP对胃肌的松弛是由VIP和NO介导的。
DOI：
10.1152/ajpgi.1993.264.4.g678
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Makhlouf,GM
中科院分区：
文献类型：
--
作者：
Jin,JG;Misra,S;Grider,JR;Makhlouf,GM
内源性速激肽[P物质（SP）和神经激肽A和B（NKA和NKB）]和受体特异性速激肽类似物（SP甲酯（SPME）、[β-Ala 8]NKA-（4-10）和senktide）的作用机制在豚鼠胃环行肌中进行了研究。交叉脱敏研究证实SPME和SP与NK-1受体相互作用，[β-Ala 8]NKA-（4-10）和NKA与NK-2受体相互作用，senktide和NKB与NK-3受体相互作用。NK-1和NK-3受体激动剂引起舒张并刺激血管活性肠肽（VIP）释放和一氧化氮（NO）产生：河豚毒素消除VIP释放、NO产生和舒张，将对NK-1受体激动剂的反应转变为收缩; NO合成酶抑制剂NG-硝基-L-精氨酸（L-NNA）可抑制NO生成，部分抑制VIP释放VIP拮抗剂VIP-（10-28）可部分抑制NO的产生阿托品可使肌松增加28-35%（P <0.01）。结果表明：（1）血管活性肠肽（VIP）和一氧化氮（NO）共同介导肌细胞的舒张;（2）VIP的释放部分依赖于一氧化氮（NO）的产生，这是由于L-NNA强烈抑制VIP的释放;（3）NO的产生主要是由于VIP对肌细胞的作用，这是由于VIP-（10-28）强烈抑制NO的释放。NK-2受体激动剂只引起不受河豚毒素影响的收缩;这些激动剂还抑制VIP释放、NO产生和NK-1和NK-3受体激动剂诱导的舒张。（250字处删节）
The mechanism of action of endogenous tachykinins [substance P (SP) and neurokinin A and B (NKA and NKB)] and of receptor-specific tachykinin analogues (SP methyl ester (SPME), [beta-Ala8]NKA-(4-10), and senktide) was examined in circular muscle of guinea pig stomach. Cross-desensitization studies confirmed that SPME and SP interacted with NK-1 receptors, [beta-Ala8]NKA-(4-10) and NKA with NK-2 receptors, and senktide and NKB with NK-3 receptors. NK-1 and NK-3-receptor agonists induced relaxation and stimulated vasoactive intestinal peptide (VIP) release and nitric oxide (NO) production: tetrodotoxin abolished VIP release, NO production, and relaxation, converting the response to NK-1-receptor agonists to contraction; the NO synthase inhibitor NG-nitro-L-arginine (L-NNA) abolished NO production, partly inhibited VIP release (56-64%, P < 0.01), and abolished relaxation; the VIP antagonist VIP-(10-28) partly inhibited NO production (73-74%, P < 0.001) and relaxation (56-58%, P < 0.01); and atropine augmented relaxation by 28-35% (P < 0.01). The pattern of inhibition implied that: 1) relaxation was mediated by VIP and NO; 2) VIP release was partly dependent on NO production, since it was strongly inhibited by L-NNA; and 3) NO was largely produced by the action of VIP on muscle cells, since it was strongly inhibited by VIP-(10-28). NK-2-receptor agonists elicited only contraction that was not affected by tetrodotoxin; these agonists also inhibited VIP release, NO production, and relaxation induced by NK-1- and NK-3-receptor agonists.(ABSTRACT TRUNCATED AT 250 WORDS)