scholarly journals The effects of angiotensin converting enzyme inhibitors and the role of the Renin-Angiotensin-Aldosterone system in J-2-N cardiomyopathic hamsters.

1992 ◽  
Vol 56 (1) ◽  
pp. 46-51 ◽  
Author(s):  
MITSUTOSHI KATO ◽  
NOBUAKIRA TAKEDA ◽  
JIE YANG ◽  
MAKOTO NAGANO
2021 ◽  
Vol 12 ◽  
Author(s):  
Annamaria Mascolo ◽  
Cristina Scavone ◽  
Concetta Rafaniello ◽  
Antonella De Angelis ◽  
Konrad Urbanek ◽  
...  

The renin-angiotensin-aldosterone system (RAAS) firstly considered as a cardiovascular circulating hormonal system, it is now accepted as a local tissue system that works synergistically or independently with the circulating one. Evidence states that tissue RAAS locally generates mediators with regulatory homeostatic functions, thus contributing, at some extent, to organ dysfunction or disease. Specifically, RAAS can be divided into the traditional RAAS pathway (or classic RAAS) mediated by angiotensin II (AII), and the non-classic RAAS pathway mediated by angiotensin 1–7. Both pathways operate in the heart and lung. In the heart, the classic RAAS plays a role in both hemodynamics and tissue remodeling associated with cardiomyocyte and endothelial dysfunction, leading to progressive functional impairment. Moreover, the local classic RAAS may predispose the onset of atrial fibrillation through different biological mechanisms involving inflammation, accumulation of epicardial adipose tissue, and electrical cardiac remodeling. In the lung, the classic RAAS regulates cell proliferation, immune-inflammatory response, hypoxia, and angiogenesis, contributing to lung injury and different pulmonary diseases (including COVID-19). Instead, the local non-classic RAAS counteracts the classic RAAS effects exerting a protective action on both heart and lung. Moreover, the non-classic RAAS, through the angiotensin-converting enzyme 2 (ACE2), mediates the entry of the etiological agent of COVID-19 (SARS-CoV-2) into cells. This may cause a reduction in ACE2 and an imbalance between angiotensins in favor of AII that may be responsible for the lung and heart damage. Drugs blocking the classic RAAS (angiotensin-converting enzyme inhibitors and angiotensin receptor blockers) are well known to exert a cardiovascular benefit. They are recently under evaluation for COVID-19 for their ability to block AII-induced lung injury altogether with drugs stimulating the non-classic RAAS. Herein, we discuss the available evidence on the role of RAAS in the heart and lung, summarizing all clinical data related to the use of drugs acting either by blocking the classic RAAS or stimulating the non-classic RAAS.


2020 ◽  
Vol 33 (3) ◽  
pp. 129-132
Author(s):  
Andre Feldman ◽  
Guilherme D’Andréa Saba Arruda ◽  
Olga Ferreira de Souza

COVID-19 is a new disease caused by the Sars-CoV-2 virus and the vast majority of patients have symptoms similar to a flu-like syndrome. A small portion of those infected ends up being hospitalized and may develop with the most severe presentation of the disease. Data from Chinese series report that hypertension appears to be a condition that imposes a greater risk of unfavorable evolution of patients. Some studies have reported that Sars-CoV-2 uses the angiotensin-converting enzyme to access its target cells. There are theories that differ about the protective or harmful role that drugs that act in the renin angiotensin aldosterone system in these patients. A British study suggests that patients using angiotensin-converting enzyme inhibitors had a lower incidence of severe forms of the disease. Another study carried out a retrospective and multicenter analysis showing that mortality was lower in the group that had used the drugs when compared to the other group (3,7 vs. 9,8%; p=0,01). The various hypotheses raised through pathophysiology are not yet able to really predict the best course of action for patients using drugs that act on the renin angiotensin system. Thus, a randomized study becomes important to try to answer definitively and with a high degree of reliability to this question.


2011 ◽  
Vol 148 (3) ◽  
pp. 377-379 ◽  
Author(s):  
Aleksandr Korniyenko ◽  
Carlos L. Alviar ◽  
Juan P. Cordova ◽  
Franz H. Messerli

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