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首页> 外文期刊>Life sciences >Nitric oxide synthase induction and relaxation in lipopolysaccharide-treated gastric fundus muscle of rats.
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Nitric oxide synthase induction and relaxation in lipopolysaccharide-treated gastric fundus muscle of rats.

机译：一氧化氮合酶在脂多糖治疗的大鼠胃底肌肉中的诱导和松弛。

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摘要

To investigate whether L-arginineitric oxide (NO) pathway activated after treatment with lipopolysaccharide (LPS) could relax the gastric fundus smooth muscle, we made functional examinations and measured NO synthase activity by the conversion of radiolabelled L-arginine to L-citrulline in rat gastric fundus strips treated with LPS in vitro. L-arginine caused a relaxation of the mucosa-free gastric fundus strips which had been treated with LPS for 6 h in vitro and then contracted by PGF2alpha beforehand. This relaxation was partially reversed by N(G)-nitro-L-arginine (a nitric oxide synthase inhibitor) or methylene blue (a soluble guanylate cyclase inhibitor). Ca(2+)-independent NO synthase activity was induced after LPS-treatment. Co-incubation with LPS and cycloheximide for 6 h inhibited the relaxation to L-arginine and the induction of NO synthase. On the other hand, Ca(2+)-dependent NO synthase activity was decreased after LPS-treatment. These results strongly suggest that Ca(2+)-independent NO synthase is induced by endotoxin in the gastric fundus muscle, resulting in inhibition of the contractile response.
机译：为了研究用脂多糖（LPS）处理后激活的L-精氨酸/一氧化氮（NO）通路能否使胃底平滑肌松弛，我们进行了功能检查，并通过将放射性标记的L-精氨酸转化为L-瓜氨酸来测定NO合酶活性。在体外用LPS处理的大鼠胃底条L-精氨酸使无粘膜胃底条松弛，该条在体外用LPS处理6小时，然后事先被PGF2alpha收缩。 N（G）-硝基-L-精氨酸（一氧化氮合酶抑制剂）或亚甲基蓝（可溶性鸟苷酸环化酶抑制剂）可部分逆转这种松弛。 LPS处理后，诱导Ca（2+）独立的NO合酶活性。与LPS和环己酰亚胺共同孵育6小时可抑制L-精氨酸的松弛和NO合酶的诱导。另一方面，LPS处理后，Ca（2+）依赖的NO合酶活性降低。这些结果强烈表明，Ca（2+）独立的NO合酶是由胃底肌内毒素诱导的，导致收缩反应的抑制。

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