Aldosterone does not mediate angiotensin II-induced atherosclerosis and abdominal aortic aneurysms

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. 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. 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. 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). These studies demonstrate that the AngII-induced vascular pathologies of atherosclerosis and AAA formation are not mediated through aldosterone.