依普利酮可抑制盐诱导的肾脏血管内皮生长因子表达。
Eplerenone suppresses salt-induced vascular endothelial growth factor expression in the kidney.
作者信息
Eatman Danita, Layas Mohammed F, Bayorh Mohamed A
机构信息
Department of Pharmacology and Toxicology, Morehouse School of Medicine, Atlanta, Ga., USA.
出版信息
Kidney Blood Press Res. 2010;33(3):167-73. doi: 10.1159/000316700. Epub 2010 Jun 23.
BACKGROUND/AIM: It is well accepted that high dietary salt intake accelerates both hypertension and target organ damage. We have previously shown that eplerenone attenuates sustained elevated systolic blood pressure in Dahl salt-sensitive (SS) rats. In the present study, we investigated the role of eplerenone on vascular endothelial growth factor (VEGF) expression because we suspected that eplerenone treatment may trigger a unique mechanism that relies on the downregulation of VEGF.
METHODS
Dahl SS rats were fed a high salt (8% NaCl) diet for 3 weeks and then switched to normal salt (0.3% NaCl) diet with or without treatment with eplerenone (100 mg/kg/day), enalapril (30 mg/kg/day) and their combination for an additional 3 weeks.
RESULTS
In addition to reducing blood pressure, eplerenone inhibited glomeruli sclerosis and suppressed the expression of VEGF and endothelial nitric oxide synthase mRNA as well as protein levels.
CONCLUSIONS
Based on these findings, we suggest that in part, VEGF stimulation of endothelial nitric oxide synthase plays a significant role in the eplerenone-induced reversal of the renal and vascular damage caused by high dietary salt intake.
背景/目的：高盐饮食会加速高血压和靶器官损伤，这一点已被广泛认可。我们之前已表明依普利酮可减轻 Dahl 盐敏感（SS）大鼠持续升高的收缩压。在本研究中，我们探究了依普利酮对血管内皮生长因子（VEGF）表达的作用，因为我们怀疑依普利酮治疗可能触发一种依赖于 VEGF 下调的独特机制。
方法
给 Dahl SS 大鼠喂食高盐（8%氯化钠）饮食 3 周，然后改为正常盐（0.3%氯化钠）饮食，并分别给予或不给予依普利酮（100 毫克/千克/天）、依那普利（30 毫克/千克/天）及其组合，再持续 3 周。
结果
除降低血压外，依普利酮还抑制肾小球硬化，并抑制 VEGF 和内皮型一氧化氮合酶 mRNA 的表达以及蛋白质水平。
结论
基于这些发现，我们认为，VEGF 对内皮型一氧化氮合酶的刺激在依普利酮诱导的、由高盐饮食引起的肾和血管损伤的逆转中发挥了重要作用。
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