Krantis A, Mattar K, Glasgow I
Digestive Diseases Research Group, University of Ottawa, Ottawa, Ontario, Canada K1H 8M5.
Am J Physiol. 1998 Nov;275(5):G897-903. doi: 10.1152/ajpgi.1998.275.5.G897.
Spontaneous relaxations occurring within motor activity in the rat gastroduodenum in vivo can be distinguished by their dependence on either nitric oxide (NO) or ATP. We examined the interaction of gamma-aminobutyric acid (GABA) and vasoactive intestinal peptide (VIP) within pathways controlling this activity in the antrum (S) and duodenum (D) of anesthetized Sprague-Dawley rats, using miniaturized extraluminal foil strain gauges oriented perpendicular to (S1, D1) or in the axis of (S2) the circular smooth muscle. The NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME; 10 mg/kg iv) attenuated (P < 0.05) antral relaxations and, in the duodenum, nonpropagating "intergroup" relaxations. The GABAA receptor antagonist bicuculline (350 micrograms/kg sc) had similar effects. The GABAA agonist 3-amino-1-propanesulfonic acid stimulated L-NAME-sensitive relaxations at S1 and D1. Propagating "grouped" responses were unchanged. VIP (6 micrograms/kg iv) always induced a relaxation of the duodenum, which was attenuated by bicuculline and L-NAME. VIP caused simultaneous responses at S1 and S2; however, the antrum displayed either contraction or relaxation in response to VIP. All antral relaxations in response to VIP were attenuated (P < 0. 05) by L-NAME; however, only VIP-induced relaxations at S1 were sensitive to bicuculline. VIP-induced contractions were also unaffected. GABAA receptors mediate the pathway(s) controlling NO-related spontaneous relaxations of the antrum and duodenal circular muscle. All VIP-induced relaxations are mediated by NO. Spontaneous relaxations of the rat gastroduodenum include responses that involve a GABAAergic NO-related pathway, which is targeted by VIP. In addition, VIP can target NO relaxations of the antrum via other pathways.
大鼠胃十二指肠在体运动活动中发生的自发性舒张可根据其对一氧化氮（NO）或三磷酸腺苷（ATP）的依赖性来区分。我们使用垂直于环形平滑肌（S1、D1）或沿其轴线（S2）方向放置的小型化腔外箔式应变片，研究了麻醉的Sprague-Dawley大鼠胃窦（S）和十二指肠（D）中控制这种活动的通路内γ-氨基丁酸（GABA）和血管活性肠肽（VIP）之间的相互作用。一氧化氮合酶抑制剂NG-硝基-L-精氨酸甲酯（L-NAME；10mg/kg静脉注射）减弱了（P<0.05）胃窦舒张以及十二指肠中不传播的“组间”舒张。GABAA受体拮抗剂荷包牡丹碱（350μg/kg皮下注射）有类似作用。GABAA激动剂3-氨基-1-丙烷磺酸在S1和D1处刺激了对L-NAME敏感的舒张。传播性“成组”反应未改变。VIP（6μg/kg静脉注射）总是引起十二指肠舒张，该舒张被荷包牡丹碱和L-NAME减弱。VIP在S1和S2处引起同步反应；然而，胃窦对VIP的反应要么是收缩要么是舒张。所有对VIP的胃窦舒张都被L-NAME减弱（P<0.05）；然而，只有VIP在S1处诱导的舒张对荷包牡丹碱敏感。VIP诱导的收缩也未受影响。GABAA受体介导控制胃窦和十二指肠环形肌与NO相关的自发性舒张的通路。所有VIP诱导的舒张均由NO介导。大鼠胃十二指肠的自发性舒张包括涉及GABAA能NO相关通路的反应，该通路是VIP的作用靶点。此外，VIP可通过其他通路作用于胃窦的NO舒张。
