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首页> 外文期刊>Life sciences >Angiotensin (1-7) contributes to nitric oxide tonic inhibition of vasopressin release during hemorrhagic shock in acute ethanol intoxicated rodents
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Angiotensin (1-7) contributes to nitric oxide tonic inhibition of vasopressin release during hemorrhagic shock in acute ethanol intoxicated rodents

机译：血管紧张素（1-7）在急性乙醇中毒啮齿动物失血性休克期间有助于一氧化氮补品抑制血管加压素的释放

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Aims Acute ethanol intoxication (AEI) attenuates the arginine vasopressin (AVP) response to hemorrhage leading to impaired hemodynamic counter-regulation and accentuated hemodynamic stability. Previously we identified that the ethanol-induced impairment of circulating AVP concentrations in response to hemorrhage was the result of augmented central nitric oxide (NO) inhibition. The aim of the current study was to examine the mechanisms underlying ethanol-induced up-regulation of paraventricular nucleus (PVN) NO concentration. Angiotensin (ANG) (1-7) is an important mediator of NO production through activation of the Mas receptor. We hypothesized that Mas receptor inhibition would decrease central NO concentration and thus restore the rise in circulating AVP levels during hemorrhagic shock in AEI rats. Main methods Conscious male Sprague-Dawley rats (300-325 g) received a 15 h intra-gastric infusion of ethanol (2.5 g/kg + 300 mg/kg/h) or dextrose prior to a fixed-pressure (~ 40 mm Hg) 60 min hemorrhage. The Mas receptor antagonist A-779 was injected through an intracerebroventricular (ICV) cannula 15 min prior to hemorrhage. Key findings PVN NOS activity and NO were significantly higher in AEI compared to DEX-treated controls at the completion of hemorrhage. ICV A-779 administration decreased NOS activity and NO concentration, partially restoring the rise in circulating AVP level at completion of hemorrhage in AEI rats. Significance These results suggest that Mas receptor activation contributes to the NO-mediated inhibitory tone of AVP release in the ethanol-intoxicated hemorrhaged host.
机译：目的急性乙醇中毒（AEI）会减弱精氨酸加压素（AVP）对出血的反应，从而导致血液动力学反调节功能受损和血液动力学稳定性增强。以前，我们确定乙醇引起的循环AVP浓度损害是由于出血引起的，这是中央一氧化氮（NO）抑制作用增强的结果。本研究的目的是研究乙醇诱导的脑室旁核（PVN）NO浓度上调的机制。血管紧张素（ANG）（1-7）是通过激活Mas受体而产生NO的重要介质。我们假设Mas受体抑制会降低AEI大鼠失血性休克过程中中央NO浓度，从而恢复循环AVP水平的升高。主要方法有意识的雄性Sprague-Dawley大鼠（300-325 g）在固定压力（〜40 mm Hg）之前接受15小时的胃内乙醇（2.5 g / kg + 300 mg / kg / h）或葡萄糖输注。 ）60分钟出血。在出血前15分钟，通过脑室内（ICV）套管注射Mas受体拮抗剂A-779。关键发现出血完成时，AEI的PVN NOS活性和NO明显高于DEX治疗的对照组。在AEI大鼠出血完成时，ICV A-779给药降低了NOS活性和NO浓度，部分恢复了循环AVP水平的升高。意义这些结果表明，在酒精中毒的出血宿主中，Mas受体激活有助于NO介导的AVP释放抑制音调。

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