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The renin-angiotensin-aldosterone system inhibitors in COVID-19: from acidosis to ventilation and immunity


Liao, Wan-Hui; Yang, Gee-Gwo; Henneberg, Maciej (2020). The renin-angiotensin-aldosterone system inhibitors in COVID-19: from acidosis to ventilation and immunity. Swiss Medical Weekly, 150:w20444.

Abstract

SARS-CoV-2 has caused a pandemic coronavirus disease 2019 (COVID-19), claiming over a million worldwide lives of people among whom those with cardiovascular disease or hypertension are over-represented. Understanding the mechanism by which coronavirus threatens human health is vital for reducing the current disease burden and even for preventing future attacks. Inspired by the temporal relationship between three coronavirus outbreaks in humans since 2000 and hypertension medications gaining popularity since 2000, we discuss here how hypertension medications might contribute to the COVID-19 pandemic and mortality with a focus on inhibitors of the renin-angiotensin-aldosterone system (RAAS). The fact that RAAS inhibitors increase angiotensin converting enzyme-2 (ACE2) expression in respiratory epithelial cells, the kidneys and heart has stirred a surge of interest in the discussion of the role of RAAS inhibitors in COVID-19 disease, all related to ACE2-mediated effects [1–5]. Here, we abstain from contributing further to this extensive discussion, but expand this discussion beyond ACE2 and centre on how RAAS blockade influences human interaction with SARS-CoV-2 by altering acid-base balance. This expansion is based on our previous experimental work conducted on aldosterone deficient mice [6] and on the fact, supported by accumulated groundwork in physiology, that acid-base homeostasis is maintained by the coordinated work of kidneys and lungs, and is vital for normal physiology and health. RAAS evolved to facilitate humans’ adaptation to land life by conserving salt and water in the intestine and kidney, and facilitating renal acid and other water-soluble waste elimination. As renal acid-excretion effects are largely dependent on the RAAS, inhibiting renal salt absorption by RAAS inhibitors in attempt to reduce blood pressure also slows renal acid elimination (see fig. 1 below).

Abstract

SARS-CoV-2 has caused a pandemic coronavirus disease 2019 (COVID-19), claiming over a million worldwide lives of people among whom those with cardiovascular disease or hypertension are over-represented. Understanding the mechanism by which coronavirus threatens human health is vital for reducing the current disease burden and even for preventing future attacks. Inspired by the temporal relationship between three coronavirus outbreaks in humans since 2000 and hypertension medications gaining popularity since 2000, we discuss here how hypertension medications might contribute to the COVID-19 pandemic and mortality with a focus on inhibitors of the renin-angiotensin-aldosterone system (RAAS). The fact that RAAS inhibitors increase angiotensin converting enzyme-2 (ACE2) expression in respiratory epithelial cells, the kidneys and heart has stirred a surge of interest in the discussion of the role of RAAS inhibitors in COVID-19 disease, all related to ACE2-mediated effects [1–5]. Here, we abstain from contributing further to this extensive discussion, but expand this discussion beyond ACE2 and centre on how RAAS blockade influences human interaction with SARS-CoV-2 by altering acid-base balance. This expansion is based on our previous experimental work conducted on aldosterone deficient mice [6] and on the fact, supported by accumulated groundwork in physiology, that acid-base homeostasis is maintained by the coordinated work of kidneys and lungs, and is vital for normal physiology and health. RAAS evolved to facilitate humans’ adaptation to land life by conserving salt and water in the intestine and kidney, and facilitating renal acid and other water-soluble waste elimination. As renal acid-excretion effects are largely dependent on the RAAS, inhibiting renal salt absorption by RAAS inhibitors in attempt to reduce blood pressure also slows renal acid elimination (see fig. 1 below).

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Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Institute of Evolutionary Medicine
Dewey Decimal Classification:610 Medicine & health
Scopus Subject Areas:Health Sciences > General Medicine
Uncontrolled Keywords:General Medicine
Language:English
Date:11 December 2020
Deposited On:18 Jan 2021 12:43
Last Modified:19 Jan 2021 21:01
Publisher:EMH Swiss Medical Publishers
ISSN:0036-7672
OA Status:Gold
Free access at:Publisher DOI. An embargo period may apply.
Publisher DOI:https://doi.org/10.4414/smw.2020.20444
PubMed ID:33306813

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