Calcium, magnesium, and oxidative stress in hyperaldosteronism.

Hyperaldosteronism has been demonstrated to be associated with magnesium loss in the urine and hypomagnesemia1 as part of the syndrome of metabolic alkalosis and hypokalemia that characterizes this condition. In this issue of Circulation, Chhokar et al2 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 the heart. This is associated with the enhanced production of reactive oxygen species (ROS) and an inflammatory phenotype, which then contribute to the decline in cardiac function and the progression to heart failure.