Local cardiac renin-angiotensin system: hypertension and cardiac failure

J Mol Cell Cardiol. 2002 Nov;34(11):1435-42. doi: 10.1006/jmcc.2002.2075.

Abstract

In addition to the effect on arterial pressure, angiotensin II, the effector peptide of the renin-angiotensin system (RAS), exerts mitogenic and growth promoting effects on cardiac myocytes and non-myocytic elements; and both of these effects significantly contribute to the development and progression of hypertensive heart disease (HHD). The traditional concept of the RAS as a systemic, endocrine system has been expanded and the identification of its components in many organs and tissue has been amassed. This paper reviews evidence that supports the concept that the cardiac RAS participate importantly in the development and risk of HHD.

Publication types

  • Review

MeSH terms

  • Aldosterone / physiology
  • Angiotensin II / physiology
  • Angiotensin-Converting Enzyme Inhibitors / pharmacology
  • Animals
  • Animals, Genetically Modified
  • Antihypertensive Agents / pharmacology
  • Heart / physiopathology*
  • Heart Failure / physiopathology*
  • Hemodynamics
  • Humans
  • Hypertension / drug therapy
  • Hypertension / physiopathology*
  • Hypertrophy, Left Ventricular / etiology
  • Hypertrophy, Left Ventricular / physiopathology
  • Myocardium / metabolism*
  • Organ Specificity
  • Rats
  • Rats, Inbred SHR
  • Renin-Angiotensin System / physiology*
  • Vascular Resistance / physiology
  • Ventricular Remodeling

Substances

  • Angiotensin-Converting Enzyme Inhibitors
  • Antihypertensive Agents
  • Angiotensin II
  • Aldosterone