Renin-angiotensin system modulators in COVID-19 patients with hypertension: friend or foe?

ABSTRACT

Background: ACE2, a component of the non-classic renin-angiotensin system (RAS), acts as a functional receptor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV 2) spike protein, which enables the entry of the virus into the host cells. Non-classical ACE2 is one of two types of ACE2 that has a protective effect on vascular and respiratory cells. RAS modulators like angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) are among the first-line treatment for hypertensive patients. An upregulation in ACE2 levels with RAS modulators was observed in few preclinical studies, which raised concerns regarding possible increased infectivity among patients treated with RAS modulators.

Method: For shortlisting the outcome effects, open-ended, English-restricted databases, published literature, and various clinical studies performed utilizing RAS modulators in COVID 19 patients were considered. 

Conclusion: Current evidence reveals no increased risk of COVID‐19 infection among hypertensive patients on ACEIs/ARBs compared to other antihypertensive medications. Several studies have demonstrated no detrimental effects of RAS modulators on clinical severity, hospital/intensive care unit stay, ventilation and mortality.  Hence, we can conclude that neither ARBs nor ACEIs treatment will cause any side effects or undesirable interactions in COVID-19 infected hypertensive patients.

KEYWORDS:

• SARS-CoV 2
• ACE2
• ACEIs
• ARBs
• ANG-II
• ANG 1-7

Acknowledgments

We are grateful to the management of Amrita School of Pharmacy, Amrita Vishwa Vidyapeetham for the support in all aspects.

Disclosure statement

We wish to confirm that there are no known conflicts of interest associated with this publication.

Author contribution

Dr. Uma Devi P designed this work, Shakhi Shylesh C M and Arya V S participated in the article preparation. Dr. Uma Devi P and Mr. Kanthlal S K critically reviewed the manuscript.

Additional information

Funding

The author(s) received no financial support for the work, authorship, and/or publication of this article.