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首页> 外文期刊>American Journal of Physiology >Differential expression of alpha2D-adrenoceptor and eNOS in aortas from early and later stages of diabetes in Goto-Kakizaki rats.
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Differential expression of alpha2D-adrenoceptor and eNOS in aortas from early and later stages of diabetes in Goto-Kakizaki rats.

机译：Goto-Kakizaki大鼠糖尿病早期和晚期的主动脉中α2D-肾上腺素能受体和eNOS的差异表达。

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摘要

The aim of the present study was to compare vascular dysfunction between the early (12 wk old) and later (36 wk old) stages of spontaneous diabetes in Goto-Kakizaki (GK) rats. We also evaluated the aortic expression of the alpha(2D)-adrenoceptor and endothelial nitric oxide synthase (eNOS). Vascular reactivity was assessed in thoracic aortas from age-matched control rats and 12- and 36-wk GK rats. Using RT-PCR and immunoblots, we also examined the changes in expression of the alpha(2D-)adrenoceptor and eNOS. In aortas from GK rats (vs. those from age-matched control rats): 1) the relaxation response to ACh was enhanced at 12 wk but decreased at 36 wk; 2) the relaxation response to sodium nitroprusside was decreased at both 12 and 36 wk, 3) norepinephrine (NE)-induced contractility was decreased at 12 wk but not at 36 wk, 4) the expressions of alpha(1B)- and alpha(1D)-adrenoceptors were unaffected, whereas those of alpha(2D)-adrenoceptor and eNOS mRNAs were increased at both 12 and 36 wk; and 5) NE- andACh-stimulated NO(x) (nitrite and nitrate) levels were increased at 12 wk, although at 36 wk ACh-stimulated NO(x) was lower, whereas NE-stimulated NO(x) showed no change. These results clearly demonstrate that enhanced ACh-induced relaxation and impaired NE-induced contraction, due to NO overproduction via eNOS and increased alpha(2D)-adrenoceptor expression, occur in early-stage GK rats and that the impaired ACh-induced relaxation in later-stage GK rats is due to reductions in both NO production and NO responsiveness (but not in eNOS expression).
机译：本研究的目的是比较Goto-Kakizaki（GK）大鼠自发性糖尿病的早期（12周龄）和晚期（36周龄）之间的血管功能障碍。我们还评估了α（2D）-肾上腺素受体和内皮一氧化氮合酶（eNOS）的主动脉表达。在年龄匹配的对照大鼠和12周和36周的GK大鼠的胸主动脉中评估血管反应性。使用RT-PCR和免疫印迹，我们还检查了alpha（2D-）肾上腺素能受体和eNOS表达的变化。在来自GK大鼠的主动脉（与年龄匹配的对照大鼠的主动脉）中：1）对ACh的松弛反应在12周时增强，而在36周时降低。 2）在12和36 wk时对硝普钠的松弛反应均下降，3）去甲肾上腺素（NE）引起的收缩力在12 wk时下降但在36 wk时没有下降，4）alpha（1B）-和alpha（ 1D）-肾上腺素受体不受影响，而α（2D）-肾上腺素受体和eNOS mRNA在12周和36周均增加; 5）NE和ACh刺激的NO（x）（亚硝酸盐和硝酸盐）水平在12周时有所增加，尽管在36周时，ACh刺激的NO（x）较低，而NE刺激的NO（x）没有变化。这些结果清楚地表明，早期的GK大鼠由于通过eNOS产生NO过量和增加的alpha（2D）-肾上腺素受体表达而导致增强的ACh诱导的松弛和受损的NE诱导的收缩，并在以后的GK大鼠中受损。阶段的GK大鼠归因于NO产生和NO反应性的降低（但eNOS表达没有降低）。

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