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首页> 外文期刊>Life sciences >Antioxidant treatment normalizes nitric oxide production, renal sodium handling and blood pressure in experimental hyperleptinemia
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Antioxidant treatment normalizes nitric oxide production, renal sodium handling and blood pressure in experimental hyperleptinemia

机译：抗氧化剂治疗可使实验性高瘦素血症中的一氧化氮生成，肾钠处理和血压正常化

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Recent studies suggest that adipose tissue hormone, leptin, is involved in the pathogenesis of arterial hypertension. However, the mechanism of hypertensive effect of leptin is incompletely understood. We investigated whether antioxidant treatment could prevent leptin-induced hypertension. Hyperleptinemia was induced in male Wistar rats by administration of exogenous leptin (0.25 mg/kg twice daily s.c. for 7 days) and separate groups were simultaneously treated with superoxide scavenger, tempol, or NAD(P)H oxidase inhibitor, apocynin (2 mM in the drinking water). After 7 days, systolic blood pressure was 20.6% higher in leptin-treated than in control animals. Both tempol and apocynin prevented leptin-induced increase in blood pressure. Plasma concentration and urinary excretion of 8-isoprostanes increased in leptin-treated rats by 66.9% and 67.7%, respectively. The level of lipid peroxidation products, malonyldialdehyde + 4-hydroxyalkenals (MDA+4-RNE), was 60.3% higher in the renal cortex and 48.1% higher in the renal medulla of leptin-treated animals. Aconitase activity decreased in these regions of the kidney following leptin administration by 44.8% and 45.1%, respectively. Leptin increased nitrotyrosine concentration in plasma and renal tissue. Urinary excretion of nitric oxide metabolites (NOx) was 57.4% lower and cyclic GMP excretion was 32.0% lower in leptin-treated than in control group. Leptin decreased absolute and fractional sodium excretion by 44.5% and 44.7%, respectively. Co-treatment with either tempol or apocynin normalized 8-isoprostanes, MDA+4-HNE, aconitase activity, nitrotyrosine, as well as urinary excretion of NOx, cGMP and sodium in rats receiving leptin. These results indicate that oxidative stress-induced NO deficiency is involved in the pathogenesis of leptin-induced hypertension. (c) 2005 Elsevier Inc. All rights reserved.
机译：最近的研究表明，脂肪组织激素瘦素与动脉高压的发病有关。然而，瘦素的高血压作用机理尚未完全了解。我们调查了抗氧化剂治疗是否可以预防瘦素诱发的高血压。雄性Wistar大鼠通过给予外源性瘦素（0.25 mg / kg每天两次，连续7天，每天两次，持续7天）诱导高瘦素血症，同时分别用超氧化物清除剂，tempol或NAD（P）H氧化酶抑制剂，载脂蛋白（2 mM饮用水）。 7天后，瘦素治疗组的收缩压比对照组动物高20.6％。 tempol和apocynin均可防止瘦素诱导的血压升高。瘦素治疗的大鼠血浆中8-异前列腺素的浓度和尿排泄分别增加了66.9％和67.7％。瘦素处理动物的肾皮质中脂质过氧化产物丙二酰二醛+ 4-羟基烯醛（MDA + 4-RNE）的水平高60.3％，在肾髓质中高48.1％。瘦素给药后，在肾脏的这些区域中乌头酸酶活性分别降低了44.8％和45.1％。瘦素增加血浆和肾脏组织中硝基酪氨酸的浓度。瘦素治疗组的一氧化氮代谢产物（NOx）尿排泄量降低57.4％，循环GMP排泄量降低32.0％。瘦素分别使绝对钠排泄和部分钠排泄减少44.5％和44.7％。在接受瘦素的大鼠中，与tempol或载脂蛋白A的共同处理可归一化8-异前列腺素，MDA + 4-HNE，乌头酸酶活性，硝基酪氨酸以及尿中NOx，cGMP和钠的排泄。这些结果表明氧化应激诱导的NO缺乏与瘦素诱导的高血压的发病机制有关。 （c）2005 Elsevier Inc.保留所有权利。

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