Pathophysiology of sodium and water retention in heart failure

Cardiology. 2001;96(3-4):122-31. doi: 10.1159/000047396.

Abstract

Heart failure is a leading cause of morbidity and mortality. In the United States, there are more than 5 million patients with heart failure and over 500,000 newly diagnosed cases each year. Numerous advances have been made in our understanding of the pathophysiologic mechanisms contributing to sodium and water retention in this condition. Important alterations in the sympathetic nervous system and the renin-angiotensin-aldosterone system have been described in heart failure, allowing the use of mechanism-specific treatments such as beta-adrenergic receptor antagonism and angiotensin-converting enzyme inhibition. As our understanding of the roles of the natriuretic peptides and the arginine vasopressin-aquaporin-2 system in the pathophysiology of heart failure evolves, treatments directed toward the alterations in these systems in heart failure can be further developed.

MeSH terms

  • Adrenergic beta-Antagonists / therapeutic use
  • Angiotensin-Converting Enzyme Inhibitors / therapeutic use
  • Atrial Natriuretic Factor / metabolism
  • Body Fluids / physiology
  • Heart Failure / drug therapy
  • Heart Failure / physiopathology*
  • Humans
  • Natriuretic Peptide, Brain / metabolism
  • Neurosecretory Systems / physiopathology
  • Renin-Angiotensin System / physiology
  • Sodium / metabolism*
  • Sympathetic Nervous System / physiopathology*
  • Vasopressins / metabolism
  • Water Intoxication / metabolism
  • Water-Electrolyte Imbalance / metabolism
  • Water-Electrolyte Imbalance / physiopathology*

Substances

  • Adrenergic beta-Antagonists
  • Angiotensin-Converting Enzyme Inhibitors
  • Vasopressins
  • Natriuretic Peptide, Brain
  • Atrial Natriuretic Factor
  • Sodium