scholarly journals The correlation between RAS and COVID-19, short review of the latest evidence

Author(s):  
F. Ferrara ◽  
A. Vitiello

Coronavirus SARS-CoV-2 is responsible for the Coronavirus disease (COVID-19) cause of the recent global pandemic, which is causing thousands of deaths worldwide and represents a health challenge with few precedents in human history. The angiotensin 2 conversion enzyme (ACE-2) has been identified as the receptor that facilitates access to SARS-CoV-2 in cells; evidence shows that its concentration varies during the various stages of viral infection. Therapeutic agents modifying the renin-angiotensin system (RAS) may be able to modulate the concentration of ACE-2 and the various components of the system. In this article we examine the latest evidence on the association between the use of RAS modifying agents and coronavirus 2019 (COVID-19) disease caused by SARS-CoV-2. Our investigation and critical literature research does not suggest discontinuation of ACEIs/ARBs treatment in clinical practice as there is a lack of robust evidence. However, we recommend further well-structured epidemiological studies investigating this sensitive issue that may provide important new suggestions for implementing guidelines.Coronavirus SARS-CoV-2 is responsible for the Coronavirus disease (COVID-19) cause of the recent global pandemic, which is causing thousands of deaths worldwide and represents a health challenge with few precedents in human history. The angiotensin 2 conversion enzyme (ACE-2) has been identified as the receptor that facilitates access to SARS-CoV-2 in cells; evidence shows that its concentration varies during the various stages of viral infection. Therapeutic agents modifying the renin-angiotensin system (RAS) may be able to modulate the concentration of ACE-2 and the various components of the system. In this article we examine the latest evidence on the association between the use of RAS modifying agents and coronavirus 2019 (COVID-19) disease caused by SARS-CoV-2. Our investigation and critical literature research does not suggest discontinuation of ACEIs/ARBs treatment in clinical practice as there is a lack of robust evidence. However, we recommend further well-structured epidemiological studies investigating this sensitive issue that may provide important new suggestions for implementing guidelines.

2016 ◽  
Vol 63 (2) ◽  
pp. 128-132
Author(s):  
Camelia C. Diaconu ◽  
◽  

Obesity is currently a true global pandemic associated with multiple co-morbidities, particularly cardiovascular, renal and metabolic diseases. There is a well-known link between obesity and hypertension, many cases of hypertension can be attributed to obesity. Reducing body weight and physical activity are important for controlling blood pressure. Currently, there are no specific guidelines about treating hypertension associated with obesity. The treatment is based on clinical experience of each physician, the knowledge of exact mechanisms of hypertension associated with obesity, comorbidities, side effects, economic reasons (cost of drugs), frequency of dosing. The majority of anti-hypertensive treatment schemes include a diuretic, an inhibitor of the renin-angiotensin system and/or a calcium channel blocker. If necessary, a mineralocorticoid receptor antagonist may be added. In patients with stage 2 hypertension a combination of two antihypertensive agents with complementary mechanisms of action is preferred. Most obese hypertensive patients need multiple antihypertensive drugs, because the prevalence of resistant hypertension is high in this population.


Author(s):  
Francesco Ferrara ◽  
Antonio Vitiello

Purpose The new coronavirus, called SARS-CoV-2, is responsible for the recent global pandemic COVID-19. The status of the global pandemic COVID-19 is currently underway, and the virus has caused about 1.11 million deaths. Several SARS-CoV-2 vaccines are in phase 3 clinical trials. Pending the availability of safe and effective vaccines, pharmacological treatments are experimental and aimed at avoiding the most serious complications of the infection. Methods This article explores and describes the scientific evidence in the literature and the scientific pharmacological and molecular rationale to consider drugs that modulate the RAS system as therapeutic agents that if administered appropriately can help the host organism to fight SARS-CoV-2 infection. Results It is known from the 2003 SARS epidemic that the critical receptor for SARS-CoV entry into host cells is the angiotensin 2 conversion enzyme (ACE2), the strain involved in the current SARS-CoV-2 epidemic is similar to the SARS-CoV strain involved in the 2002-2003 SARS epidemic. ACE-2 is part of the RAS system, the modulation of this enzyme could be of therapeutic efficacy. Conclusion Depending on pharmacological knowledge, and epidemiological evidence in the literature based on current knowledge of the mechanism of penetration of SARS-CoV-2 in cells, and the role of ACE-2 in the inflammatory state of infection, therapeutic treatments that modulate RAS could be a weapon to fight COVID-19 infection.


2020 ◽  
Vol 11 (SPL1) ◽  
pp. 957-962
Author(s):  
Amar Prashad Chaudhary ◽  
Adna Nelson K ◽  
Jamuna T R

The emergence of COVID-19, the global pandemic is originated from the Nobel member of the family, i.e. SARS-COV-2 initially seen at Wuhan city of China since December 2019 have deeply impacted the lives of people and changed the way of our living. The pandemic has led to the death of thousands of people mostly seen in old age people, people having co-morbidity like cardiovascular disease, diabetes , obesity, kidney disease, etc. and cigarette smokers. It is found that cigarette smokers are more prone to the COVID-19 infection and have more severity of the disease when infected. From various studies, it has been revealed that there is increased pulmonary ACE2 expression in ever smokers and virus leading to an imbalance in the RAS appears to be an important cause for cigarette smokers which is being impacted more in this pandemic. This review article explains the underlying mechanism why smokers are more prone to COVID-19? why higher severity of the disease is higher in them?


Author(s):  
Mansour Adam Mahmoud

Background: COVID-19 is considered the most challenging global pandemic. Patients with COVID-19 are more vulnerable to renal impairment especially those admitted to the Intensive Care Units (ICUs). Objective: In this review we discuss the epidemiology, the pathophysiology, the clinical implications and specific COVID-19 therapy in CKD patients. Results: The prevalence of CKD patients with COVID-19 varies between 0.7 to 47.6%. Patients with CKD ought to be encouraged to take extra precautions (isolation, distancing, wearing Personal Protective Equipment (PPE)) to limit the risk of exposure to the virus. Renin-Angiotensin System (RAS) and SARS-CoV-2 interactions, through the binding of the virus to ACE-2, have  produced speculations of both likely damage and advantage of RAS inhibitor use during the pandemic. Remidisivir should be avoided in CKD patients (Cr Cl<30ml/min) with COVID-19. In addition, the doses of nephrotoxic medications (chloroquine phosphate and dexamethasone) that are recommended to be used in the management of COVID-19 should be adjusted according to creatinine clearance and dialysis. Conclusion: COVID-19 may worsen the impaired kidney function and increase mortality.                Care givers should pay especial attention to medications dosing in COVID-19 patient with CKD history.


2021 ◽  
Vol 11 (4) ◽  
pp. 1497
Author(s):  
Darina Bačenková ◽  
Marianna Trebuňová ◽  
Tatiana Špakovská ◽  
Marek Schnitzer ◽  
Lucia Bednarčíková ◽  
...  

The global pandemic known as coronavirus disease 2019 (COVID-19) was caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). This review article presents the taxonomy of SARS-CoV-2 coronaviruses, which have been classified as the seventh known human pathogenic coronavirus. The etiology of COVID-19 is also briefly discussed. Selected characteristics of SARS-CoV-2, SARS-CoV, and HCoV-NL63 are compared in the article. The angiotensin converting enzyme-2 (ACE-2) has been identified as the receptor for the SARS-CoV-2 viral entry. ACE2 is well-known as a counter-regulator of the renin-angiotensin system (RAAS) and plays a key role in the cardiovascular system. In the therapy of patients with COVID-19, there has been a concern about the use of RAAS inhibitors. As a result, it is hypothesized that ACE inhibitors do not directly affect ACE2 activity in clinical use. Coronaviruses are zoonotic RNA viruses. Identification of the primary causative agent of the SARS-CoV-2 is essential. Sequencing showed that the genome of the Bat CoVRaTG13 virus found in bats matches the genome of up to (96.2%) of SARS-CoV-2 virus. Sufficient knowledge of the molecular and biological mechanisms along with reliable information related to SARS-CoV-2 gives hope for a quick solution to epidemiological questions and therapeutic processes.


Author(s):  
G. Mazzocchi ◽  
P. Rebuffat ◽  
C. Robba ◽  
P. Vassanelli ◽  
G. G. Nussdorfer

It is well known that the rat adrenal zona glomerulosa steroidogenic activity is controlled by the renin-angiotensin system. The ultrastructural changes in the rat zona glomerulosa cells induced by renovascular hypertension were described previously, but as far as we are aware no correlated biochemical and morphometric investigations were performed.Twenty adult male albino rats were divided into 2 experimental groups. One group was subjected to restriction of blood flow to the left kidney by the application of a silver clip about the left renal artery. The other group was sham-operated and served as a control. Renovascular hypertension developed in about 10 days: sistolic blood pressure averaged 165 ± 6. 4 mmHg, whereas it was about 110 ± 3. 8 mmHg in the control animals. The hypertensive and control rats were sacrificed 20 days after the operation. The blood was collected and plasma renin activity was determined by radioimmunological methods. The aldosterone concentration was radioimmunologically assayed both in the plasma and in the homogenate of the left capsular adrenal gland.


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