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首页> 外文期刊>Life sciences >Nebivolol does not protect against 5/6 ablation/infarction induced chronic kidney disease in rats - Comparison with angiotensin II receptor blockade
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Nebivolol does not protect against 5/6 ablation/infarction induced chronic kidney disease in rats - Comparison with angiotensin II receptor blockade

机译：奈必洛尔不能预防5/6消融/梗塞诱发的大鼠慢性肾脏疾病-与血管紧张素II受体阻滞剂的比较

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Aims: Nitric oxide (NO) deficiency contributes to chronic kidney disease progression. Nebivolol, a beta adrenergic receptor antagonist, may enhance endogenous NO. Here, we investigated whether Nebivolol attenuates hypertension and renal injury after 5/6 ablation/infarction (A/I). Efficacy was compared to the AT1 receptor antagonist Olmesartan. Main methods: Kidney disease and hypertension were induced by right kidney ablation and ~ 2/3 infarction of the left kidney. Rats were treated orally with vehicle (placebo), Nebivolol (5 mg/kg b.i.d.), or Olmesartan (2.5 mg/kg/day) for 6 weeks after A/I. Key findings: With placebo, glomerular sclerosis and tubulointersititial fibrosis developed with increased blood pressure and proteinuria, and a fall in NO x excretion. Olmesartan prevented these changes, but Nebivolol had no effect on these measures but lowered heart rate. Neither treatment reduced systemic oxidative stress (urinary hydrogen peroxide and TBARS). Compared to controls, renal cortex abundance of nNOSα decreased and nNOSβ increased in rats after 5/6 A/I, with no changes in eNOS. Neither treatment restored nNOSα; however, both reduced nNOSβ. Activity of DDAH was decreased by 5/6 A/I but restored by both treatments despite no increase in DDAH protein abundance. Kidney cortex abundance of manganese SOD fell after 5/6 A/I and was restored by treatment with Olmesartan but not Nebivolol. Extracellular and copper/zinc SOD abundances were not changed. Significance: In conclusion, Nebivolol showed no benefit after 6 weeks in rapidly progressing, ANG II-dependent 5/6 A/I model of chronic kidney disease. This contrasts to the protection seen with 6 month treatment of Nebivolol in the slowly progressing 5/6 ablation model.
机译：目的：一氧化氮（NO）缺乏症会导致慢性肾脏疾病的进展。 Nebivolol，一种β肾上腺素能受体拮抗剂，可能会增强内源性NO。在这里，我们研究了奈比洛尔在5/6消融/梗塞（A / I）后是否能减轻高血压和肾脏损伤。将功效与AT1受体拮抗剂奥美沙坦进行了比较。主要方法：右肾消融和左肾的约2/3梗塞可诱发肾脏疾病和高血压。 A / I后，用赋形剂（安慰剂），奈必洛尔（5 mg / kg b.i.d.）或奥美沙坦（2.5 mg / kg /天）口服处理大鼠6周。主要发现：服用安慰剂后，肾小球硬化和肾小管间质纤维化发展，血压和蛋白尿增加，NOx排泄下降。奥美沙坦阻止了这些改变，但奈必洛尔对这些措施没有影响，但降低了心率。两种治疗均不能降低全身性氧化应激（尿过氧化氢和TBARS）。与对照组相比，在5/6 A / I后，大鼠肾皮质nNOSα的丰度降低而nNOSβ的升高，而eNOS没有变化。两种治疗均未恢复nNOSα。然而，两者均降低了nNOSβ。 DDAH的活性降低了5/6 A / I，但是尽管DDAH蛋白的丰度没有增加，但两种处理均恢复了DDAH的活性。 5/6 A / I后，锰SOD的肾脏皮层丰度下降，通过奥美沙坦（而非奥美沙坦）治疗可恢复。细胞外和铜/锌超氧化物歧化酶的丰度没有改变。启示：总的来说，奈比洛尔在快速发展的，依赖于ANG II的5/6 A / I模型慢性肾脏疾病的6周后没有显示出任何益处。这与在缓慢进展的5/6消融模型中使用奈比洛尔6个月治疗所见的保护作用相反。

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