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The mechanisms of vasorelaxant effect of leptin on isolated rabbit aorta.

机译:瘦素对离体兔主动脉血管舒张作用的机制。

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摘要

In the present study, we analysed the effects of leptin on rabbit aorta and the mechanisms underlying these effects. Leptin (10(-12)-10(-9) m) induced concentration-dependent relaxation in intact rabbit aorta rings precontracted with phenylephrine (10(-6) m). Removal of endothelium abolished the effects of leptin. Pretreatment of rings with N(omega)-nitro-l-arginine methyl ester (10(-4) m 20 min) or catalase (1200 U/mL 20 min) significantly reduced the relaxant response to leptin when compared with the control group. The incubation of brefeldin A (3.5 x 10(-5) m 90 min), indomethacin (10(-5) m 20 min), tetraethylammonium (10(-4) m 20 min), and glibenclamide (10(-5) m, 20 min) did not affect the leptin-induced vasodilation. These results suggest that leptin relaxes the rabbit aorta. The relaxation is mediated by endothelium-derived nitric oxide and hydrogen peroxide.
机译:在本研究中,我们分析了瘦素对兔主动脉的作用及其潜在机制。瘦素(10(-12)-10(-9)m)在与去氧肾上腺素(10(-6)m)预收缩的完整兔主动脉环中诱导浓度依赖性的松弛。去除内皮消除了瘦素的作用。与对照组相比,用N(ω)-硝基-1-精氨酸甲酯(10(-4)m 20分钟)或过氧化氢酶(1200 U / mL 20分钟)预处理环显着降低了对瘦素的松弛反应。布雷菲德菌素A(3.5 x 10(-5)m 90分钟),消炎痛(10(-5)m 20分钟),四乙铵(10(-4)m 20分钟)和格列苯脲(10(-5)的孵育,20分钟)不影响瘦素诱导的血管舒张。这些结果表明瘦素使兔主动脉松弛。松弛是由内皮衍生的一氧化氮和过氧化氢介导的。

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