Ames Marisa K, Atkins Clarke E, Pitt Bertram
Department of Clinical Sciences, College of Veterinary Medicine, Colorado State University, Fort Collins, Colorado.
Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina.
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.
肾素-血管紧张素-醛固酮系统（RAAS）的慢性激活会促使充血性心力衰竭、系统性高血压和慢性肾病综合征的发生并使之持续存在。循环系统和组织中血管紧张素II（AngII）及醛固酮水平过高会导致促纤维化、促炎症及促肥厚的环境，进而引起心血管和肾组织的重塑及功能障碍。在过去几十年里，人们对RAAS在这种异常病理重塑中的作用的认识不断加深，并且已经开发出了许多旨在抑制RAAS的药物疗法。尽管如此，这些疾病的发病率仍然很高。对RAAS复杂性的持续研究应有助于临床医生调节（抑制或增强）该系统的组成部分，从而提高生活质量和生存率。这篇综述重点介绍了我们对RAAS以及AngII和醛固酮过量的病理生理学的最新认识，回顾了在心血管和肾脏疾病（尤其是猫和狗）中关于抑制RAAS的已知情况。
