Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Oxidative stress in aldosteronism.

Yao Sun1, Robert A Ahokas, Syamal K Bhattacharya

  • 1Department of Medicine, Division of Cardiovascular Diseases, University of Tennessee Health Science Center, 920 Madison Ave., Suite 300, Memphis, 38163, USA.

Cardiovascular Research
|April 25, 2006
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Validity of International Classification of Diseases (ICD)-9 and ICD-10 Codes for Medication-Related Osteonecrosis of the Jaw (MRONJ) Among Individuals Prescribed Antiresorptives for Fracture Prevention Across Two Cohorts.

Clinical epidemiology·2026
Same author

Activation of sarco/endoplasmic reticulum Ca²⁺-ATPase 2 (SERCA2) reduces brain injury and improves cognitive function following ischemic stroke.

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie·2026
Same author

Management of glucocorticoid-induced osteoporosis in rheumatic diseases.

Best practice & research. Clinical rheumatology·2026
Same author

Mortality Following Atypical Femoral Fractures in Men.

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research·2026
Same author

Performance of U.S.- FRAX TM by Race and Ethnicity for Short-term Hip and Major Osteoporotic Fracture Prediction in U.S. Women with Rheumatoid Arthritis.

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research·2026
Same author

Heart Failure is an Independent Risk Factor for Incident Hip, Proximal Humerus, and Wrist Fractures in a High-Risk Older Population.

Journal of general internal medicine·2026
Same journal

Metabolic crisis and TRPM4 activation cause QT prolongation in TANGO2 deficiency disorder.

Cardiovascular research·2026
Same journal

Personalizing Atrial Fibrillation Therapy: Moving from Genetic Association to Mechanistic Translation.

Cardiovascular research·2026
Same journal

Placental Growth Factor Promotes Endothelial Activation and Inflammatory Remodelling in Pulmonary Hypertension.

Cardiovascular research·2026
Same journal

Endothelial-to-mesenchymal transition (EndMT) in atherosclerosis: mechanisms, models and therapies.

Cardiovascular research·2026
Same journal

The gut-heart axis in cardio-oncology.

Cardiovascular research·2026
Same journal

Proteomic signatures as biomarkers of atherosclerosis burden.

Cardiovascular research·2026
See all related articles

Congestive heart failure involves systemic illness, oxidative stress, and bone wasting. Aldosteronism contributes to this by altering cation levels, leading to secondary hyperparathyroidism and further oxidative stress, suggesting nutritional management may help.

Area of Science:

  • Cardiology
  • Biochemistry
  • Nutritional Science

Background:

  • Congestive heart failure (CHF) is a systemic illness characterized by oxidative stress, inflammation, and tissue wasting, beyond cardiac dysfunction.
  • Aldosteronism, a key neurohormonal factor in CHF, promotes an altered redox state and cation imbalances (Ca2+, Mg2+).
  • Secondary hyperparathyroidism in CHF is exacerbated by aldosteronism-induced cation loss and loop diuretic use, contributing to oxidative stress via a 'calcium paradox'.

Purpose of the Study:

  • To explore the role of aldosteronism, divalent cations (calcium, magnesium), and oxidative stress in the pathophysiology of congestive heart failure.
  • To investigate the mechanisms linking aldosteronism, secondary hyperparathyroidism, and oxidative stress in CHF.
  • To evaluate the potential of nutritional interventions, including macro- and micronutrients, as complementary management strategies for CHF.

Related Experiment Videos

Main Methods:

  • Review of existing literature on the pathophysiology of congestive heart failure, focusing on neurohormonal profiles, oxidative stress markers, and mineral metabolism.
  • Analysis of the interplay between aldosteronism, parathyroid hormone (PTH) secretion, and divalent cation homeostasis (Ca2+, Mg2+) in CHF.
  • Examination of the impact of pharmacological interventions (spironolactone, amlodipine, N-acetylcysteine) and surgical options (parathyroidectomy) on CHF-related pathophysiology.

Main Results:

  • Aldosteronism contributes to CHF progression by increasing urinary and fecal excretion of Ca2+ and Mg2+, leading to hypocalcemia and hypomagnesemia.
  • Elevated PTH levels in response to low Ca2+ and Mg2+ drive bone resorption and contribute to oxidative stress through intracellular Ca2+ overload (calcium paradox).
  • Pharmacological agents like spironolactone, amlodipine, and N-acetylcysteine, along with parathyroidectomy, show potential in mitigating these adverse effects.

Conclusions:

  • Congestive heart failure involves complex systemic processes including oxidative stress and mineral imbalances driven by aldosteronism.
  • Secondary hyperparathyroidism in CHF is a significant contributor to oxidative stress and may be influenced by nutritional status and medication.
  • Nutritional management, targeting macro- and micronutrients, presents a promising complementary approach to pharmaceutical therapies for CHF.