Heart and liver mitochondria isolated from rats treated with enalapril, 3-30 mg/kg/day in the drinking water for 7-120 days, showed a time- and dose-dependent increased nitric oxide (NO) production in the range of 14-250%. Heart and liver mitochondria from control rats produced 0.69 and 0.50 nmol of NO/min/mg of protein, respectively, as determined by dual wavelength spectrophotometry (577-591 nm) following hemoglobin oxidation to methemoglobin. The response to enalapril treatment, attributed to a gene-mediated up-regulation of mitochondrial nitric oxide synthase (mtNOS) activity, was half-maximal at 5-6 days and was maintained up to 120 days. Enalapril-treated animals showed an increased mtNOS functional activity in heart mitochondria that inhibited state 3 O(2) uptake (from 22% in control rats to 43%) and increased state 4 hydrogen peroxide (H(2)O(2)) production (from 30% in control rats to 52%). Calculated heart intramitochondrial NO and H(2)O(2) steady-state concentrations were increased 66% and 20%, respectively, by enalapril treatment. Signaling pathways dependent on mitochondrial NO and H(2)O(2) may account for the beneficial effects of enalapril in aging mammals.

译文

:从依那普利以3-30 mg / kg / day在饮用水中处理7-120天的大鼠分离的心脏和肝线粒体显示出时间和剂量依赖性的一氧化氮(NO)产生量在14范围内增加-250%。血红蛋白氧化为高铁血红蛋白后,通过双波长分光光度法(577-591 nm)测定,对照大鼠的心脏和肝线粒体分别产生0.69和0.50 nmol的NO / min / mg蛋白。归因于基因介导的线粒体一氧化氮合酶(mtNOS)活性上调的依那普利治疗反应在5-6天达到最大一半,并维持至120天。依那普利治疗的动物在心脏线粒体中表现出增加的mtNOS功能活性,从而抑制状态3 O(2)的摄取(从对照大鼠的22%增至43%)并增加了状态4的过氧化氢(H(2)O(2))的产生(从对照组的30%增至52%)。通过依那普利治疗,计算出的心脏线粒体内NO和H(2)O(2)稳态浓度分别增加了66%和20%。依赖线粒体NO和H(2)O(2)的信号通路可能解释了依那普利在衰老哺乳动物中的有益作用。

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