Motor responses in rat ileum evoked by nitric oxide donors vs. field stimulation: modulation by pituitary adenylate cyclase-activating peptide, forskolin and guanylate cyclase inhibitors.
Motor responses in rat ileum evoked by nitric oxide donors vs. field stimulation: modulation by pituitary adenylate cyclase-activating peptide, forskolin and guanylate cyclase inhibitors.
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一氧化氮供体引起的大鼠回肠运动反应与场刺激：垂体腺苷酸环化酶激活肽、毛喉素和鸟苷酸环化酶抑制剂的调节。
DOI：
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发表时间：
1997
影响因子：
3.5
通讯作者：
F. Sundler
中科院分区：
文献类型：
--
作者：
E. Ekblad;F. Sundler
本研究探讨了一氧化氮（NO）介导的影响，纵向肌肉与贴壁肌间神经节从大鼠回肠在体外使用NO供体和电场刺激。电场刺激（20 Hz）引起双相反应-舒张后收缩。NG-硝基-L-精氨酸甲酯几乎完全消除了这种舒张作用，而L-精氨酸使之恢复，收缩作用不受影响。NO供体钠-亚硝基-N-乙酰青霉胺（SNAP）和硝普钠也诱导了双相反应，收缩后舒张。亚甲基蓝或1H-[1，2，4]恶二唑并[4，3-a]-喹喔啉-1-酮不能阻断神经元释放的NO介导的舒张，这表明它们不依赖于细胞内环状鸟苷酸环化酶的升高。它们的振幅不受毛喉素的影响。从SNAP释放的NO（或NO相关物质）引起的舒张被亚甲蓝或1H-[1，2，4]恶二唑[4，3-a]-喹喔啉-1-酮阻断，表明环鸟苷酸环化酶依赖性作用机制。腺苷酸环化酶激活肽和毛喉素，而不是血管活性肠肽或神经肽Y，引起了SNAP诱导的舒张的浓度-反应曲线的显着漂移。SNAP引起的收缩可被亚甲蓝和1H-[1，2，4]恶二唑并[4，3-a]喹喔啉-1-酮阻断，因此呈环鸟苷酸环化酶依赖性。SNAP引起的收缩被垂体腺苷酸环化酶激活肽和forskolin所消除，但不受血管活性肠肽或NPY的影响。总之，由NO供体释放的NO与神经释放的NO引起的运动反应揭示了不同的作用机制。
This study examines nitric oxide (NO) mediated effects on longitudinal muscle with adherent myenteric ganglia from rat ileum in vitro using NO donors and electrical field stimulation. Electrical field stimulation (20 Hz) caused a biphasic response-a relaxation followed by a contraction. NG-nitro-L-arginine methyl ester almost totally abolished the relaxation and L-arginine restored it. The contraction was unaffected. The NO donors sodium-nitroso-N-acetylpenicillamine (SNAP) and sodium-nitroprusside also induced a biphasic response, a contraction followed by relaxation. Relaxations mediated by neuronally released NO were not blocked by methylene blue or 1H-[1,2,4]oxadiazolo[4,3-a]-quinoxalin-1-one suggesting that they are independent of a rise in intracellular cyclic guanylate cyclase. Their amplitude was unaffected by forskolin. The relaxations evoked by NO (or a NO-related substance) liberated from SNAP were blocked by methylene blue or 1H-[1,2,4]oxadiazolo[4,3-a]-quinoxalin-1-one indicating a cyclic guanylate cyclase-dependent mechanism of action. Pituitary adenylate cyclase-activating peptide and forskolin, but not vasoactive intestinal peptide or neuropeptide Y, caused a marked leftward shift of the concentration-response curve of the SNAP-induced relaxation. The contractions induced by SNAP were blocked by methylene blue and 1H-[1,2,4]oxadiazolo[4,3-a]-quinoxalin-1-one and thus, cyclic guanylate cyclase dependent. The SNAP-induced contractions were abolished by pituitary adenylate cyclase-activating peptide and forskolin, but unaffected by vasoactive intestinal peptide or NPY. In conclusion, motor responses evoked by NO released from NO donors vs. neuronally released NO reveals different mechanisms of action.
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