Involvement of nitric oxide in endothelium-dependent arterial relaxation by leptin
Involvement of nitric oxide in endothelium-dependent arterial relaxation by leptin
复制标题
DOI：
10.1006/bbrc.2000.3005
复制
发表时间：
2000-07-05
影响因子：
3.1
通讯作者：
Nishio, I
中科院分区：
文献类型：
--
作者：
Kimura, K;Tsuda, K;Nishio, I
瘦素是一种多肽，主要在白色脂肪组织中产生，可增强交感神经活性。一些研究调查了瘦素对外周血管的影响。我们检测了人瘦素对大鼠动脉的血管松弛作用。用1×10~(-6)m ol/L的苯肾上腺素预收缩动脉环，并灌流瘦素，瘦素以剂量依赖的方式松弛去氧肾上腺素预收缩的动脉环。ED_(50)为8.4微克/毫升，去除内皮细胞后，瘦素的作用消失。吲哚美辛(1×10~(-5)m ol/L)不影响瘦素的血管舒缩作用，而N-奥米伽-硝基-L精氨酸甲酯(L-NAME)的1×10~(-4)m o l/L可完全抑制瘦素的舒血管作用。这种抑制作用可被1×10~(-4)摩尔/L的L-精氨酸拮抗。在K通道阻滞剂的灌流过程中，瘦素正常地松弛动脉环，包括格列本脲3×10(-5)m ol/L，1×10(-6)m ol/L apamin和5×10(-7)m ol/L。低氯溶液(8.3 mm o l/L)可抑制瘦素引起的血管松弛，但硝普钠对血管内皮非依赖性的扩张作用不受影响。这些结果提示，瘦素对动脉的松弛作用是由内皮细胞释放的一氧化氮介导的，而氯离子在瘦素诱导的一氧化氮释放中起重要作用。(C)2000年学术出版社。
Leptin is a polypeptide, mainly produced in white adipose tissue, and increases sympathetic nerve activity. A few studies investigated leptin's effect on peripheral vessels. We examined the vasorelaxant effects of human leptin on rat arteries. Arterial rings were precontracted with 1 x 10(-6) mol/l of phenylephrine, and leptin was superfused, Leptin relaxed phenylephrine-precontracted arterial rings in a dose-dependent manner. ED50 was calculated to 8.4 mu g/ml. Removal of endothelium abolished the effects of leptin. Indomethacin (1 x 10(-5) mol/l) did not affect the vasorelaxation by leptin, whereas 1 x 10(-4) mol/l of N-omega-nitro-L-arginine methyl ester (L-NAME) completely suppressed it. The inhibition was antagonized by 1 x 10(-4) mol/l of L-arginine. Leptin normally relaxed arterial rings during superfusion of K channel blockers, including 3 x 10(-5) mol/l of glibenclamide, 1 x 10(-6) of mol/l apamin, and 5 x 10(-7) mol/l of charybdotoxin. Low Cl- solution (8.3 mmol/l) inhibited leptin-induced relaxation, but endothelium-independent vasodilatation by nitroprusside was not impaired at law Cl- solution. These results suggest that arterial relaxation by leptin is mediated by nitric oxide released from endothelium, and Cl- plays an important role in leptin-induced nitric oxide release. (C) 2000 Academic Press.