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首页> 外文期刊>Research communications in molecular pathology and pharmacology >Glycyrrhetinic acid-sensitive mechanism does not make a major contribution to non-prostanoid, non-nitric oxide mediated endothelium-dependent relaxation of rat mesenteric artery in response to acetylcholine.
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Glycyrrhetinic acid-sensitive mechanism does not make a major contribution to non-prostanoid, non-nitric oxide mediated endothelium-dependent relaxation of rat mesenteric artery in response to acetylcholine.

机译：甘草次酸的敏感性机制对非前列腺素，非一氧化氮介导的大鼠肠系膜动脉对乙酰胆碱的舒张作用没有重大贡献。

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Pharmacological characteristics of non-prostanoid (PGI2), non-NO mediated endothelium-dependent relaxation in response to acetylcholine (ACh) were examined in the isolated rat mesenteric artery, especially focusing on the possible contribution of the gap junctional communication in the response. ACh produced an endothelium-dependent relaxation of the isolated rat mesenteric artery with functional endothelium in the presence of both indomethacin (3 x 10(-6) M) and N(G)-nitro-L-arginine methyl ester (L-NAME) (10(-4) M), an inhibitor of nitric oxide synthase (NOS). ACh-induced relaxation of the rat mesenteric artery in the presence of indomethacin and L-NAME was strongly attenuated in the solution containing high (80 mM) KCl, tetraethylammonium (TEA) (10(-2) M), which suggests the involvement of endothelium-derived relaxing factor(s) (EDHF(s)) in the response. Non-PGI2, non-NO mediated endothelium-dependent relaxation to ACh was not profoundly affected by glibenclamide (10(-6) M), 4-aminopyridine (4-AP) (10(-4) M), iberiotoxin (10(-7) M), agitoxin-2 (10(-8) M), or apamin (10(-7) M), but was abolished by the treatment with apamin (10(-7) M) plus charybdotoxin (10(-7) M). Non-PGI2, non-NO mediated endothelium-dependent relaxation to ACh was not substantially affected by arachidonic acid (AA) (10(-4) M) or ONO-RS-082 (10(-5) M), an inhibitor of phospholipase A2, which rules out the involvement of AA metabolites in the vascular response. Furthermore, a gap junction inhibitor, 18alpha-glycyrrhetinic acid (18alpha-GA) did not show dramatic inhibitory effect on non-PGI2, non-NO mediated endothelium-dependent relaxation induced by ACh. These findings suggest that 1) metabolites of AA are not involved in non-PGI2, non-NO mediated endothelium-dependent relaxation to ACh in the isolated rat mesenteric artery; 2) Heterocellular gap junctional communication does not mainly account for non-PGI2, non-NO mediated endothelium-dependent relaxation evoked by ACh in this artery.
机译：在分离的大鼠肠系膜动脉中检查了非前列腺素（PGI2），非NO介导的对乙酰胆碱（ACh）的内皮依赖性舒张的药理学特征，尤其关注了间隙连接通讯在反应中的可能贡献。在吲哚美辛（3 x 10（-6）M）和N（G）-硝基-L-精氨酸甲酯（L-NAME）均存在的情况下，ACh产生具有功能性内皮的离体大鼠肠系膜动脉的内皮依赖性舒张（10（-4）M），一氧化氮合酶（NOS）的抑制剂。在含有吲哚美辛和L-NAME的情况下，ACh诱导的大鼠肠系膜动脉松弛在含有高（80 mM）KCl，四乙铵（TEA）（10（-2）M）的溶液中被大大减弱，这表明内皮源性舒张因子（EDHF）。非PGI2，非NO介导的ACh内皮依赖性舒张不受格列本脲（10（-6）M），4-氨基吡啶（4-AP）（10（-4）M），埃博毒素（10（ -7）M），agitoxin-2（10（-8）M）或阿帕明（10（-7）M），但通过用阿帕明（10（-7）M）加charybdotoxin（10（7（ -7）M）。花生四烯酸（AA）（10（-4）M）或ONO-RS-082（10（-5）M）（一种PPAR2的抑制剂）对ACh的非PGI2，非NO介导的内皮依赖性舒张作用基本上没有影响磷脂酶A2，可排除AA代谢产物参与血管反应。此外，间隙连接抑制剂18α-甘草次酸（18alpha-GA）对ACh诱导的非PGI2，非NO介导的内皮依赖性舒张作用未显示出显着的抑制作用。这些发现表明：1）在分离的大鼠肠系膜动脉中，AA的代谢产物不参与非PGI2，非NO介导的内皮依赖性对ACh的舒张; 2）异细胞间隙连接通讯并不主要解释ACh在该动脉中引起的非PGI2，非NO介导的内皮依赖性舒张。

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