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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Mechanisms underlying the nitric oxide inhibitory effects in mouse ileal longitudinal muscle.
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Mechanisms underlying the nitric oxide inhibitory effects in mouse ileal longitudinal muscle.

机译：一氧化氮在小鼠回肠纵向肌肉中抑制作用的潜在机制。

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摘要

We investigated the mechanisms involved in the nitric oxide (NO)-induced inhibitory effects on longitudinal smooth muscle of mouse ileum, using organ bath technique. Exogenously applied NO, delivered as sodium nitroprusside (SNP; 0.1–100 micromol/L) induced a concentration-dependent reduction of the ileal spontaneous contractions. 1H-[1,2,4]oxadiazolol[4,3,a]quinoxalin-1-one (ODQ; 1 micromol/L), a guanilyl cyclase inhibitor, reduced the SNP-induced effects. Tetraethylammonium chloride (20 mmol/L), a non-selective K+ channel blocker, and charybdotoxin (0.1 micromol/L), blocker of large conductance Ca2+-dependent K+ channels, significantly reduced SNP-induced inhibitory effects. In contrast, apamin (0.1 micromol/L), blocker of small conductance Ca2+-dependent K+ channels, was not able to affect the response to SNP. Ciclopiazonic acid (10 micromol/L) or thapsigargin (0.1 micromol/L), sarcoplasmatic reticulum Ca2+-ATPase inhibitors, decreased the SNP-inhibitory effects. Ryanodine (10 micromol/L), inhibitor of Ca2+ release from ryanodine-sensitive intracellular stores, significantly reduced the SNP inhibitory effects. The membrane permeable analogue of cGMP, 8-bromoguanosine 3′,5′-cyclic monophosphate (100 micromol/L), also reduced spontaneous mechanical activity, and its effect was antagonized by ryanodine. The present study suggests that NO causes inhibitory effects on longitudinal smooth muscle of mouse ileum through cGMP which in turn would activate the large conductance Ca2+-dependent K+ channels, via localized ryanodine-sensitive Ca2+ release.
机译：我们使用器官浴技术研究了一氧化氮（NO）诱导的对小鼠回肠纵向平滑肌抑制作用的机制。外源施用的NO，以硝普钠（SNP; 0.1–100 micromol / L）的形式传递，导致回肠自发性收缩的浓度依赖性降低。鸟苷酸环化酶抑制剂1H- [1,2,4]恶二唑[4,3，a]喹喔啉-1-酮（ODQ; 1 micromol / L）降低了SNP诱导的作用。四乙胺氯化铵（20 mmol / L），一种非选择性的K +通道阻滞剂，以及甲壳毒素（0.1 micromol / L），一种大电导Ca2 +依赖性K +通道的阻滞剂，显着降低了SNP诱导的抑制作用。相比之下，小传导性Ca2 +依赖性K +通道的阻滞剂apamin（0.1 micromol / L）不能影响对SNP的反应。环孢酮酸（10 micromol / L）或thapsigargin（0.1 micromol / L），肌浆网Ca2 + -ATPase抑制剂可降低SNP抑制作用。 Ryanodine（10 micromol / L）是抑制从雷诺丁敏感的细胞内存储中释放Ca2 +的抑制剂，大大降低了SNP的抑制作用。 cGMP的膜渗透性类似物8-溴鸟苷3'，5'-环一磷酸酯（100 micromol / L）也降低了自发的机械活性，并且其作用被ryanodine拮抗。本研究表明，NO可以通过cGMP对小鼠回肠的纵向平滑肌产生抑制作用，而cGMP则可以通过局部性的雷诺丁碱敏感的Ca2 +释放来激活大电导的Ca2 +依赖性K +通道。

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