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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Modulation of vasomotion in resistance arteries of JCR:LA-cp rats: a model of insulin resistance.
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Modulation of vasomotion in resistance arteries of JCR:LA-cp rats: a model of insulin resistance.

机译:JCR:LA-cp大鼠抵抗动脉中血管运动的调节:胰岛素抵抗模型。

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Obesity and insulin resistance are strongly associated with an increased risk of vascular disease. Vasomotion is the cyclic variation in the diameter of arteries and is a general feature of the vasculature that may have important physiological consequences. We tested the hypothesis that obesity - insulin resistance is associated with abnormal vasomotion by comparing obese, insulin-resistant JCR:LA-cp rats, known to develop vasculopathy, atherosclerosis, and ischemic lesions of the heart, with lean insulin-sensitive animals from the same strain. Vasomotion was assessed using isolated mesenteric arteries on a myograph system after preconstriction to 50% of maximal constriction with norepinephrine. The amplitude of vasomotion was enhanced by the presence of meclofenamate, a prostaglandin H synthase inhibitor, and was diminished by N(G)-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor. Removal of the endothelium essentially abolished vasomotion, and meclofenamate had no effect on de-endothelialized arteries. Frequency was not altered by either L-NAME or meclofenamate. Although pharmacological inhibition of nitric oxide and eicosanoid production clearly altered vasomotion, there was no difference in the amplitude or frequency of vasomotion in arteries from obese rats compared with lean rats. These results indicate that the endothelium plays a central role in modulating vasomotion, involving both enhancing and inhibiting effects, and that vasomotion is similar between obese, insulin-resistant and lean, insulin-sensitive rats.
机译:肥胖和胰岛素抵抗与血管疾病的风险增加密切相关。血管运动是动脉直径的周期性变化,是脉管系统的一般特征,可能会产生重要的生理后果。我们通过比较肥胖,胰岛素抵抗性JCR:LA-cp大鼠(已知会发展为血管病,动脉粥样硬化和心脏缺血性病变)与瘦弱的胰岛素敏感性动物,检验了肥胖-胰岛素抵抗与异常血管运动有关的假设。相同的应变。用去甲肾上腺素预先收缩至最大收缩量的50%后,使用肌电图系统上的孤立的肠系膜动脉评估血管舒张功能。血管收缩的幅度因前列腺素H合酶抑制剂甲氯芬那酸酯的存在而增加,而一氧化氮合酶抑制剂N(G)-硝基-L-精氨酸甲酯(L-NAME)则减弱了。去除内皮基本上消除了血管运动,而甲氯芬那酸酯对去内皮的动脉没有影响。 L-NAME或甲氯芬那酸酯均未改变频率。尽管一氧化氮和类二十烷酸产生的药理学抑制作用明显改变了血管运动,但是与瘦大鼠相比,肥胖大鼠动脉的血管运动幅度或频率没有差异。这些结果表明,内皮在调节血管运动中起着中心作用,涉及增强和抑制作用,并且肥胖,胰岛素抵抗和瘦的,胰岛素敏感性大鼠的血管运动相似。

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