Obesity-associated activation of angiotensin and endothelin in the cardiovascular system

Int J Biochem Cell Biol. 2003 Jun;35(6):826-37. doi: 10.1016/s1357-2725(02)00307-2.

Abstract

The renin-angiotensin system (RAS) and the endothelin system have been implicated in the pathogenesis of human cardiovascular and renal diseases, and inhibition of the RAS markedly improves morbidity and survival. Obesity in humans is associated with an increased risk for the development of hypertension, atherosclerosis and focal-segmental glomerulosclerosis, however the exact mechanisms underlying these pathologies in obese individuals are not known. This article discusses the clinical importance of obesity and the current evidence for local activation of the renin-angiotensin system and its interactions with the endothelin system in obesity and the cardiovascular pathologies associated with it.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adipocytes / metabolism
  • Adiponectin
  • Angiotensin II / metabolism
  • Animals
  • Endothelin-1 / metabolism
  • Endothelium, Vascular / physiology*
  • Hormones, Ectopic / metabolism
  • Humans
  • Hypertension / etiology
  • Hypertension / physiopathology*
  • Insulin Resistance
  • Intercellular Signaling Peptides and Proteins*
  • Kidney / metabolism
  • Leptin / metabolism
  • Mice
  • Nerve Growth Factor
  • Obesity / complications
  • Obesity / physiopathology*
  • Proteins / metabolism
  • Rats
  • Renin-Angiotensin System / physiology*
  • Resistin

Substances

  • Adiponectin
  • Endothelin-1
  • Hormones, Ectopic
  • Intercellular Signaling Peptides and Proteins
  • Leptin
  • Proteins
  • RETN protein, human
  • RETNLB protein, human
  • Resistin
  • Retn protein, mouse
  • Retn protein, rat
  • Retnla protein, mouse
  • Retnla protein, rat
  • Angiotensin II
  • Nerve Growth Factor