Calcium, Magnesium, and Oxidative Stress in Hyperaldosteronism "...Our knowledge of the (patho)physiological role of aldosterone and that of magnesium has increased dramatically during the past few years. The finding that aldosterone acts on target tissues other than the classic epithelial cells (kidney, colon) has had a profound influence on our understanding of the significance of aldosterone in cardiovascular disease. Aldosterone is now known to act on the heart and blood vessels, not only on muscle (smooth muscle and cardiomyocytes), but also on endothelial cells, where it induces nuclear swelling,3 which has been implicated in the mechanisms of vascular damage. Part of the effects of aldosterone may be mediated by the upregulation of endothelin-1 gene expression in the vasculature and the heart,4 as well as cross-talk with endothelin ETA receptors at the level of caveolae/lipid rafts.5 These effects occur through different mechanisms that may involve NADPH oxidase,6 xanthine oxidase,7 or mitochondrial sources of ROS,8 which result in the increased generation of free radicals. Increased oxidant stress may activate inflammatory mediators nuclear factor-?B and activator protein-1, which upregulate adhesion molecules and result in the vascular inflammatory phenotype...." read more: http://m.circ.ahajournals.org/content/111/7/830.full


Circulation
m.circ.ahajournals.org
In this issue of Circulation , Chhokar et al 2 demonstrate the consequences of metabolic changes in rats subjected to aldosterone infusion in the presence of excess salt that result in hypocalcemia and hypomagnesemia, hyperparathyroidism, bone resorption, and calcium overload of tissues including th…