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一氧化氮在空腹胃底张力及5-羟色胺1受体介导的胃底舒张中的作用

Role of nitric oxide in fasting gastric fundus tone and in 5-HT1 receptor-mediated relaxation of gastric fundus.

作者信息

Coulie B, Tack J, Sifrim D, Andrioli A, Janssens J

机构信息

Center for Gastroenterological Research, University Hospital Gasthuisberg, Catholic University of Leuven, B-3000 Louvain, Belgium.

出版信息

Am J Physiol. 1999 Feb;276(2):G373-7. doi: 10.1152/ajpgi.1999.276.2.G373.

DOI:10.1152/ajpgi.1999.276.2.G373
PMID:9950810
Abstract

Fasting gastric fundus tone is maintained by continuous cholinergic input. 5-Hydroxytryptamine-1 (5-HT1) receptor activation decreases gastric fundus tone in humans. Whether this fundus-relaxing effect is mediated via inhibition of cholinergic input or via activation of a nitrergic pathway is unknown. The aim of the present study was to determine the effect of nitrergic inhibition on feline gastric fundus tone and on 5-HT1 receptor-mediated relaxation of the fundus. Administration of Nomega-nitro-L-arginine methyl ester (L-NAME) alone caused a significant decrease of the mean baseline volume (P < 0.005), which was restored completely by addition of L-arginine. Sumatriptan caused a dose-dependent relaxation of the gastric fundus (P < 0.0005). This relaxation was inhibited by L-NAME (P < 0.02) and was restored by prior administration of L-arginine. Buspirone did not cause any change in mean baseline volume, whereas the sumatriptan-induced relaxation was not affected by prior administration of NAN-190. Our data indicate that fasting fundus tone relies not only on continuous cholinergic input but also on continuous nitrergic input, implying that fasting fundus tone is maintained by the balance of a cholinergic and nitrergic drive. Furthermore, fundus relaxation via 5-HT1 receptor activation is mediated through activation of a nitrergic pathway.

摘要

空腹时胃底张力由持续的胆碱能输入维持。5-羟色胺-1(5-HT1)受体激活可降低人类胃底张力。这种胃底松弛效应是通过抑制胆碱能输入还是通过激活一氧化氮能途径介导尚不清楚。本研究的目的是确定一氧化氮能抑制对猫胃底张力以及对5-HT1受体介导的胃底松弛的影响。单独给予N-甲基-L-精氨酸甲酯(L-NAME)可使平均基线容积显著降低(P<0.005),加入L-精氨酸后可完全恢复。舒马曲坦可引起胃底剂量依赖性松弛(P<0.0005)。这种松弛被L-NAME抑制(P<0.02),且预先给予L-精氨酸可恢复。丁螺环酮对平均基线容积无任何影响,而舒马曲坦诱导的松弛不受预先给予NAN-190的影响。我们的数据表明,空腹时胃底张力不仅依赖于持续的胆碱能输入,还依赖于持续的一氧化氮能输入,这意味着空腹时胃底张力由胆碱能和一氧化氮能驱动的平衡维持。此外,通过5-HT1受体激活引起的胃底松弛是通过一氧化氮能途径的激活介导的。

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