Young H M, Ciampoli D, Johnson P J, Stebbing M J
Department of Anatomy and Cell Biology, University of Melbourne, Parkville, Vic., Australia.
J Auton Nerv Syst. 1996 Nov 6;61(2):103-8. doi: 10.1016/s0165-1838(96)00064-1.
In this work we describe a region of mouse intestine, the caecum, in which inhibitory transmission to the longitudinal muscle is predominantly due to nitric oxide. In the presence of muscarinic receptor blockade, electrical stimulation of intramural nerves in the longitudinal muscle of the mouse caecum evoked a relaxation. The relaxation was reduced to about 25% of the control amplitude by the nitric oxide synthase inhibitor L-NMMA (NG-methyl-L-arginine), but was unaffected by D-NMMA. In the presence of the nitric oxide scavenger oxyhaemoglobin, the relaxation was reduced to less than 10% of the control amplitude. In the circular muscle of the caecum and the longitudinal muscle of the ileum, colon and rectum, electrical field stimulation either evoked only small relaxations, or relaxations that were unaffected by L-NMMA. Nitric oxide synthase-containing neurons in the caecum were localized immunohistochemically using an antibody to neuronal nitric oxide synthase or with NADPH diaphorase histochemistry. Reactive nerve cell bodies were observed in the myenteric plexus, and varicose nerve fibres were present in the longitudinal and circular muscle layers of the caecum. The transduction mechanism of the nitric oxide-mediated relaxation in the longitudinal muscle of the caecum was examined using ODQ (1 H-[1,2,4]oxadiazolo[4,3,-alpha-]quinoxalin-1-one), a selective inhibitor of soluble guanylyl cyclase. ODQ abolished the relaxations induced by applied sodium nitroprusside (0.01-1 mM) and reduced the relaxation induced by electrical stimulation to about 40% of control values. However, ODQ reduced the relaxations induced by electrical stimulation to a lesser extent than L-NMMA. Hence, although the relaxation in this tissue mediated by NO (or an NO-related substance) is largely via soluble guanylyl cyclase, an action of NO on other targets cannot be ruled out.
在本研究中，我们描述了小鼠肠道的一个区域——盲肠，其中对纵肌的抑制性传递主要归因于一氧化氮。在毒蕈碱受体阻断的情况下，电刺激小鼠盲肠纵肌中的壁内神经会引起舒张。一氧化氮合酶抑制剂L-NMMA（NG-甲基-L-精氨酸）可使舒张幅度降低至对照幅度的约25%，但D-NMMA对其无影响。在存在一氧化氮清除剂氧合血红蛋白的情况下，舒张幅度降低至对照幅度的不到10%。在盲肠的环肌以及回肠、结肠和直肠的纵肌中，电场刺激要么仅引起微小的舒张，要么引起不受L-NMMA影响的舒张。使用抗神经元型一氧化氮合酶抗体或通过NADPH黄递酶组织化学，对盲肠中含一氧化氮合酶的神经元进行免疫组织化学定位。在肌间神经丛中观察到反应性神经细胞体，盲肠的纵肌层和环肌层中存在曲张神经纤维。使用可溶性鸟苷酸环化酶的选择性抑制剂ODQ（1H-[1,2,4]恶二唑并[4,3-α]喹喔啉-1-酮）研究了盲肠纵肌中一氧化氮介导的舒张的转导机制。ODQ消除了硝普钠（0.01 - 1 mM）引起的舒张，并将电刺激引起的舒张降低至对照值的约40%。然而，ODQ对电刺激引起的舒张的降低程度小于L-NMMA。因此，尽管该组织中由NO（或与NO相关的物质）介导的舒张在很大程度上是通过可溶性鸟苷酸环化酶进行的，但不能排除NO对其他靶点的作用。
