Endothelial damage and regeneration: the role of the renin-angiotensin-aldosterone system

Curr Hypertens Rep. 2011 Feb;13(1):86-92. doi: 10.1007/s11906-010-0171-x.

Abstract

The renin-angiotensin-aldosterone system (RAAS) is part of the blood pressure regulating system. Its main effector peptide is angiotensin II (Ang II). Although it may induce hypertension, the proinflammatory, profibrotic, and prothrombotic effects are mainly mediated by effects of Ang II on the cellular and molecular level that are independent of blood pressure. Therefore, pharmacotherapeutic intervention within the RAAS is an important treatment modality for patients suffering from cardiovascular diseases, even those who are not hypertensive. In addition to the blood pressure lowering and vasculoprotective (pleiotropic) effects of angiotensin II type 1 (AT(1)) receptor blockers (ARBs), and angiotensin-converting enzyme (ACE) inhibitors, regenerative progenitor cell therapy emerges as an auxiliary therapy to improve regeneration of the vascular endothelium. This review focuses on the growing knowledge about regenerating vascular cells, their response to RAAS effectors, and RAAS-modulating pharmacotherapy in the context of endothelial cell damage and regeneration.

Publication types

  • Review

MeSH terms

  • Angiotensin II / antagonists & inhibitors
  • Angiotensin II / drug effects*
  • Angiotensin II Type 1 Receptor Blockers / therapeutic use
  • Angiotensin-Converting Enzyme Inhibitors / therapeutic use*
  • Antihypertensive Agents / therapeutic use*
  • Endothelium, Vascular / drug effects*
  • Endothelium, Vascular / pathology
  • Humans
  • Hypertension / drug therapy*
  • Hypertension / pathology
  • Reactive Oxygen Species
  • Renin / antagonists & inhibitors
  • Renin / drug effects
  • Renin-Angiotensin System / drug effects*
  • Risk Factors
  • Stem Cells

Substances

  • Angiotensin II Type 1 Receptor Blockers
  • Angiotensin-Converting Enzyme Inhibitors
  • Antihypertensive Agents
  • Reactive Oxygen Species
  • Angiotensin II
  • Renin