The role of renin–angiotensin system inhibition in the treatment of hypertension in metabolic syndrome: are all the angiotensin receptor blockers equal?

2007 ◽  
Vol 11 (2) ◽  
pp. 191-205 ◽  
Author(s):  
Asterios Karagiannis ◽  
Dimitri P Mikhailidis ◽  
Vasilios G Athyros ◽  
Anna I Kakafika ◽  
Konstantinos Tziomalos ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Angiotensin Receptor Blockers ◽  
Renin Angiotensin System ◽  
Angiotensin Receptor ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Treatment Of Hypertension ◽  
Receptor Blockers

scholarly journals Renin-Angiotensin-System (RAS) und COVID-19 – Zur Verordnung von RAS-Blockern

2020 ◽  
Vol 145 (10) ◽  
pp. 682-686 ◽  
Author(s):  
Reinhold Kreutz ◽  
Engi Abd El-Hady Algharably ◽  
Detlev Ganten ◽  
Franz Messerli
Keyword(s):  
Angiotensin Receptor Blockers ◽  
Renin Angiotensin System ◽  
Short Review ◽  
Angiotensin Receptor ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Analysis And Evaluation ◽  
Receptor Blockers ◽  
Ras Blockers ◽  
Regulatory Functions

AbstractTwenty years ago, an enzyme homologous to the previously known angiotensin-converting enzyme (ACE) was identified, and subsequently named ACE2. In the renin-angiotensin system (RAS), ACE2 has counter-regulatory functions against the classical effector peptide angiotensin II, for example in blood pressure regulation and cardiovascular remodeling. However, ACE2 provides an initially unexpected interesting link between virology and cardiovascular medicine. That is, ACE2 represents the binding receptor for the cellular uptake of SARS-CoV and SARS-CoV-2 viruses. Thus, ACE2 is relevant for COVID-19. In this context, it was suspected that therapy with RAS blockers might promote transmission and complications of COVID-19 by upregulation of ACE2 expression. The aim of this short review is, to describe the link between the RAS, particularly ACE2, and COVID-19. Based on our analysis and evaluation of the available findings, we justify our conclusion: important drugs such as ACE inhibitors and angiotensin receptor blockers should continue to be prescribed according to guidelines to stable patients in the context of the COVID-19 pandemic.

scholarly journals Acute Kidney Injury in a Case Series of Patients with Confirmed COVID-19 (Coronavirus Disease 2019): Role of Angiotensin-Converting Enzyme 2 and Renin-Angiotensin System Blockade

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Avantika Chenna ◽  
Venu Madhav Konala ◽  
Subhasish Bose ◽  
Sasmit Roy ◽  
Bhaskar Reddy Madhira ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Angiotensin Converting Enzyme ◽  
Angiotensin Receptor Blockers ◽  
Kidney Injury ◽  
Renin Angiotensin System ◽  
Converting Enzyme ◽  
Angiotensin Receptor ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Receptor Blockers

The renin-angiotensin system plays a very critical role in hypertension, diabetes, and kidney and heart diseases. The blockade of the renin-angiotensin system results in the prevention of progression of renal and cardiac damage. There have been controversial hypotheses raised regarding the safety of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in COVID-19 (coronavirus disease 2019). We present the case series of four patients (2 men and 2 women; 1 Caucasian and 3 African Americans; two survived and two died) with confirmed COVID-19, presenting with respiratory symptoms and acute kidney injury, who have been on angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. Membrane-bound angiotensin-converting enzyme 2 (ACE2) has been implicated as the gateway for viral entry into the human cell in causing the infection. The factors contributing to acute kidney injury are diuretics, iodinated contrast administration, hemodynamic instability apart from ACE inhibitors, and angiotensin receptor blockers. The ACE inhibitors and ARBs were stopped in these patients due to acute kidney injury. We also discussed the role of ACE2 and the renin-angiotensin system (RAS) blockade in patients with COVID-19 infection along with pathogenesis.

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