The renin-angiotensin-aldosterone system and its suppression

J Vet Intern Med. 2019 Mar;33(2):363-382. doi: 10.1111/jvim.15454. Epub 2019 Feb 26.


Chronic activation of the renin-angiotensin-aldosterone system (RAAS) promotes and perpetuates the syndromes of congestive heart failure, systemic hypertension, and chronic kidney disease. Excessive circulating and tissue angiotensin II (AngII) and aldosterone levels lead to a pro-fibrotic, -inflammatory, and -hypertrophic milieu that causes remodeling and dysfunction in cardiovascular and renal tissues. Understanding of the role of the RAAS in this abnormal pathologic remodeling has grown over the past few decades and numerous medical therapies aimed at suppressing the RAAS have been developed. Despite this, morbidity from these diseases remains high. Continued investigation into the complexities of the RAAS should help clinicians modulate (suppress or enhance) components of this system and improve quality of life and survival. This review focuses on updates in our understanding of the RAAS and the pathophysiology of AngII and aldosterone excess, reviewing what is known about its suppression in cardiovascular and renal diseases, especially in the cat and dog.

Keywords: angiotensin converting enzyme inhibitor; angiotensin receptor blocker; chronic kidney disease; heart failure; mineralocorticoid receptor blocker; proteinuric kidney disease; systemic hypertension.

Publication types

  • Review

MeSH terms

  • Aldosterone / metabolism
  • Angiotensin II / metabolism
  • Angiotensin Receptor Antagonists / therapeutic use
  • Angiotensin-Converting Enzyme Inhibitors / therapeutic use*
  • Animals
  • Cat Diseases / drug therapy*
  • Cat Diseases / physiopathology
  • Cats
  • Dog Diseases / drug therapy*
  • Dog Diseases / physiopathology
  • Dogs
  • Heart Failure / veterinary
  • Hypertension / veterinary
  • Kidney Diseases / veterinary
  • Mineralocorticoid Receptor Antagonists / therapeutic use
  • Renin-Angiotensin System / drug effects*
  • Renin-Angiotensin System / physiology


  • Angiotensin Receptor Antagonists
  • Angiotensin-Converting Enzyme Inhibitors
  • Mineralocorticoid Receptor Antagonists
  • Angiotensin II
  • Aldosterone