Aldosterone does not mediate angiotensin II-induced atherosclerosis and abdominal aortic aneurysms
Aldosterone does not mediate angiotensin II-induced atherosclerosis and abdominal aortic aneurysms
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DOI：
10.1038/sj.bjp.0706098
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发表时间：
2005-02-01
影响因子：
7.3
通讯作者：
Daugherty, A
中科院分区：
文献类型：
--
作者：
Cassis, LA;Helton, MJ;Daugherty, A
1我们以前已经证明，血管紧张素II（AngII）输注到高血压小鼠中会增加动脉粥样硬化并导致腹主动脉瘤（AAA）的形成。本研究的目的是确定醛固酮在这些血管紧张素II诱导的血管病变中的作用。2雄性载脂蛋白E-/-（apoE）小鼠输注溶媒或醛固酮（50或200 ng kg（-1）min（-1））。在整个研究过程中测定动脉血压，并在输注28天后定量血清脂质浓度和血管病理学。3输注醛固酮不影响体重或血清胆固醇浓度。通过输注醛固酮，肾脏重量呈剂量依赖性增加。醛固酮对收缩压无明显影响。通过输注醛固酮，血浆醛固酮浓度呈剂量依赖性增加。然而，醛固酮对动脉粥样硬化的程度没有影响，也没有形成AAA。4在AngII灌注的apoE-/-小鼠（1000 ng kg（-1）min（-1））中植入含有螺内酯的颗粒（16 mg kg（-1）d（-1））对AngII诱导的血压升高没有影响。血浆醛固酮浓度不受安体舒通与血管紧张素II共同管理。螺内酯给药不影响动脉粥样硬化的程度。此外，安体舒通对AngII诱导的AAA没有显著影响（AAA形成的发生率：溶媒组与安体舒通组分别为80%和70%;不显著）。5这些研究表明AngII诱导的动脉粥样硬化和AAA形成的血管病理学不是通过醛固酮介导的。
1 We have demonstrated previously that infusion of angiotensin II (AngII) into hyperlipidemic mice augments atherosclerosis and results in the formation of abdominal aortic aneurysms ( AAA). The purpose of this study was to determine the role of aldosterone in these AngII-induced vascular pathologies.2 Male apolipoprotein E-/- (apoE) mice were infused with either vehicle or aldosterone (50 or 200 ng kg(-1) min(-1)). Arterial blood pressure was determined throughout the study and serum lipid concentrations and vascular pathology were quantified after 28 days of infusion.3 Infusion of aldosterone did not influence body weight or serum cholesterol concentrations. Kidney weight was increased dose-dependently by aldosterone infusion. Systolic blood pressure was not significantly altered by aldosterone. Plasma aldosterone concentrations were increased dose-dependently by infusion of aldosterone. However, there was no effect of aldosterone on the extent of atherosclerosis and AAAs were not formed.4 Implantation of pellets containing spironolactone (16 mg kg(-1) day(-1)) in AngII-infused apoE-/- mice (1000 ng kg(-1) min(-1)) had no effect on AngII-induced elevations in blood pressure. Plasma aldosterone concentration was not influenced by coadministration of spironolactone with AngII. Spironolactone administration did not influence the extent of atherosclerosis. Moreover, spironolactone had no significant effect on AngII-induced AAA (incidence of AAA formation: 80 versus 70% for vehicle versus spironolactone, respectively; not significant).5 These studies demonstrate that the AngII-induced vascular pathologies of atherosclerosis and AAA formation are not mediated through aldosterone.