| Institution: | 1. https://orcid.org/0000-0002-3865-6123;2. Department of Clinical Sciences, College of Veterinary Medicine, Colorado State University, Fort Collins, Colorado;3. Marisa K. Ames, Department of Clinical Sciences, Colorado State University College of Veterinary Medicine and Biomedical Sciences, 1678 Campus Deliver, Fort Collins, CO 80523.;4. Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina;5. Department of Medicine, University of Michigan School of Medicine, Ann Arbor, Michigan |
| Abstract: | 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. |
