Abstract
Congestive heart failure (CHF) is more than a failing heart and salt-avid state. Also present is a systemic illness which features oxidative stress in diverse tissues, a proinflammatory phenotype, and a wasting of soft tissue and bone. Reactive oxygen and nitrogen species contribute to this illness and the progressive nature of CHF. Aldosteronism, an integral component of the neurohormonal profile found in CHF, plays a permissive role in leading to an altered redox state. Because of augmented urinary and fecal excretion of Ca(2+) and Mg(2+) and consequent decline in plasma-ionized [Ca(2+)](o) and [Mg(2+)](o) that accompanies aldosteronism, parathyroid glands release parathyroid hormone (PTH) in an attempt to restore Ca(2+) and Mg(2+) homeostasis; this includes bone resorption. However, PTH-mediated intracellular Ca(2+) overloading, considered a Ca(2+) paradox, leads to oxidative stress. This can be prevented by: spironolactone, an aldosterone receptor antagonist that rescues urinary and fecal cation losses; parathyroidectomy; amlodipine, a Ca(2+) channel blocker; N-acetylcysteine, an antioxidant. In addition to the role played by aldosteronism in the appearance of secondary hyperparathyroidism is the chronic use of a loop diure...Continue Reading
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