The renin‐angiotensin‐aldosterone system and its suppression
Autor: | Clarke E. Atkins, Marisa K. Ames, Bertram Pitt |
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Rok vydání: | 2019 |
Předmět: |
medicine.medical_specialty
040301 veterinary sciences Reviews heart failure Review Aldosterone levels 030204 cardiovascular system & hematology Small Animal 0403 veterinary science 03 medical and health sciences chemistry.chemical_compound Endocrinology 0302 clinical medicine Internal medicine Renin–angiotensin system Medicine angiotensin receptor blocker mineralocorticoid receptor blocker Aldosterone General Veterinary business.industry systemic hypertension 04 agricultural and veterinary sciences medicine.disease Angiotensin II Pathophysiology chemistry proteinuric kidney disease Heart failure Cardiology angiotensin converting enzyme inhibitor business chronic kidney disease Kidney disease |
Zdroj: | Journal of Veterinary Internal Medicine |
ISSN: | 1939-1676 0891-6640 |
DOI: | 10.1111/jvim.15454 |
Popis: | 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. |
Databáze: | OpenAIRE |
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