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Effects of nesfatin-1 on atrial contractility and thoracic aorta reactivity in male rats

机译:nesfatin-1对雄性大鼠心房收缩性和胸主动脉反应性的影响

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Background: This study aimed to examine the effects of nesfatin-1 on thoracic aorta vasoreactivity and to investigate the inotropic and chronotropic effects of nesfatin-1 on the spontaneous contractions of the isolated rat atria.Methods: Isolated right atria and thoracic aorta were used in organ baths. The reactivity of the thoracic aorta was evaluated by potassium chloride (KCI), phenylephrine (Phe), acetylcholine (ACh), and sodium nitroprusside (SNP). The effects of nesfatin-1 on the spontaneous contractions of the rat atria were also examined.Results: Nesfatin-1 (0.1-100 ng/ml) produced a concentration-dependent relaxation response in rat thoracic aorta. The relaxant responses to nesfatin-1 were inhibited by the removal of endothelium, NO synthase blocker N-nitro-L-arginine methyl ester (L-NAME, 10-4 M), and soluble guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, 10“5 M). Nesfatin-1 (10 ng/ml, 30 min) increased the relaxation responses to either ACh or SNP, and the contractile response to both Phe and KCI did not significantly change in the arteries that were incubated with nesfatin-1 compared with the controls. The thoracic aorta contractions induced by the stepwise addition of Ca2+ to a high KCI solution with no Ca2+ were not significantly changed by nesfatin-1. Under calcium-free conditions, the contractions of the thoracic aorta rings incubated with nesfatin-1 in response to Phe were not significantly lower than those of the rings from the control rats. Nesfatin-1 showed positive inotropic and chronotropic effects on rat atria.Conclusion: Nesfatin-1 significantly changed the vascular responsiveness in rat thoracic aorta and produced positive inotropic and chronotropic effects on rat atria.
机译:背景:本研究旨在检测Nesfatin-1对胸部主动脉血管反应性的影响,并研究Nesfatin-1对孤立鼠Atria的自发性收缩的尿液和正慢效应。方法:孤立的右心塔和胸主动脉器官浴。通过氯化钾(KCl),苯妥还研究了Nesfatin-1对大鼠阿里亚亚洲的自发收缩的影响。结果:Nesfatin-1(0.1-100ng / ml)在大鼠胸主动脉中产生浓度依赖性的松弛响应。通过去除内皮酸抑制对Nesfatin-1的松弛反应,没有合成酶阻滞剂N-NITRO-L-精氨酸甲酯(L-NAME,10-4 M)和可溶性胍基环化酶抑制剂1H- [1,2, 4]氧基亚唑[4,3-A]喹喔啉-1-一(ODQ,10“5米)。 Nesfatin-1(10ng / ml,30分钟)增加了对ACH或SNP的弛豫响应,并且对照与NESFATIN-1相比,对PHE和KCI的收缩反应没有显着变化,与对照组相比。 NESFATIN-1没有显着改变由逐步加入CA2 +至高KCl溶液的胸主动脉凹陷,NESFATIN-1未显着改变。在无钙条件下,与NESFATIN-1响应PHE孵育的胸部主动脉环的收缩并没有明显低于来自对照大鼠的环的重点。 Nesfatin-1显示对大鼠阿里亚氏症的正矫肌和正潮疗效。结论:Nesfatin-1显着改变了大鼠胸主动脉的血管反应性,并产生了对大鼠阿里亚患者的正滴管和正交效应。

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