Oxidative stress in aldosteronism

Yao Sun, Robert A. Ahokas, Syamal K. Bhattacharya, Ivan C. Gerling, Laura D Carbone, Karl T. Weber

Research output: Contribution to journalReview article

32 Citations (Scopus)

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 Ca2+ and Mg2+ and consequent decline in plasma-ionized [Ca2+]o and [Mg2+]o that accompanies aldosteronism, parathyroid glands release parathyroid hormone (PTH) in an attempt to restore Ca2+ and Mg2+ homeostasis; this includes bone resorption. However, PTH-mediated intracellular Ca2+ overloading, considered a Ca2+ 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 Ca2+ 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 diuretic, which further enhances urinary Ca2+ and Mg2+ excretion, and reduced Ca2+ stores associated with hypovitaminosis D. This broader perspective of CHF and the ever increasing clinical relevance of divalent cations and oxidative stress raise the question of their potential management with macro- and micronutrients. An emerging body of evidence suggests the nutritional management of CHF offers an approach that will be complementary to today's pharmaceutical-based strategies.

Original languageEnglish (US)
Pages (from-to)300-309
Number of pages10
JournalCardiovascular Research
Volume71
Issue number2
DOIs
StatePublished - Jul 15 2006
Externally publishedYes

Fingerprint

Hyperaldosteronism
Oxidative Stress
Heart Failure
Parathyroid Hormone
Mineralocorticoid Receptor Antagonists
Sodium Potassium Chloride Symporter Inhibitors
Reactive Nitrogen Species
Amlodipine
Parathyroidectomy
Secondary Hyperparathyroidism
Parathyroid Glands
Micronutrients
Divalent Cations
Acetylcysteine
Bone Resorption
Oxidation-Reduction
Cations
Reactive Oxygen Species
Homeostasis
Salts

Keywords

  • Aldosterone
  • Calcium
  • Magnesium
  • Oxidative stress
  • Parathyroid hormone

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Sun, Y., Ahokas, R. A., Bhattacharya, S. K., Gerling, I. C., Carbone, L. D., & Weber, K. T. (2006). Oxidative stress in aldosteronism. Cardiovascular Research, 71(2), 300-309. https://doi.org/10.1016/j.cardiores.2006.03.007

Oxidative stress in aldosteronism. / Sun, Yao; Ahokas, Robert A.; Bhattacharya, Syamal K.; Gerling, Ivan C.; Carbone, Laura D; Weber, Karl T.

In: Cardiovascular Research, Vol. 71, No. 2, 15.07.2006, p. 300-309.

Research output: Contribution to journalReview article

Sun, Y, Ahokas, RA, Bhattacharya, SK, Gerling, IC, Carbone, LD & Weber, KT 2006, 'Oxidative stress in aldosteronism', Cardiovascular Research, vol. 71, no. 2, pp. 300-309. https://doi.org/10.1016/j.cardiores.2006.03.007
Sun Y, Ahokas RA, Bhattacharya SK, Gerling IC, Carbone LD, Weber KT. Oxidative stress in aldosteronism. Cardiovascular Research. 2006 Jul 15;71(2):300-309. https://doi.org/10.1016/j.cardiores.2006.03.007
Sun, Yao ; Ahokas, Robert A. ; Bhattacharya, Syamal K. ; Gerling, Ivan C. ; Carbone, Laura D ; Weber, Karl T. / Oxidative stress in aldosteronism. In: Cardiovascular Research. 2006 ; Vol. 71, No. 2. pp. 300-309.
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