Could ACE inhibitors, and particularly ARBs, Increase susceptibility to COVID-19 infection
It has been established that the ACE2 receptor is the entry point for COVID-19.
The ACE2 receptor acts as an Angiotensin 2 (AT2) converter to into the vasodilator and antitrophic heptapeptide, angiotensin-(1–7).
It has 60% homology with ACE1 receptor but ACE inhibitors have no ACE2 activity.
Angiotensin Receptor Blockers (ARBs) block AT2 receptors and increase circulating Angiotensin 2 levels approximately 6 fold.
A paper published in Circulation in 2005(ref) showed that ACE Inhibitors increase cardiac ACE2 receptor mRNA significantly and ACE2 levels less significantly.
ARBs were shown to increase both ACE2 mRNA and to more than double cardiac ACE2 levels.
Both of these drug classes are very widely prescribed. It can be reasonably hypothesised that ARBs, and to a lesser extent ACE inhibitors, could potentially increase the levels of ACE2 receptors in type 2 Pneumocytes - the putative entry point of COVID 19 to lung tissue. Could this potentially lead to increased viral load and more severe lung injury?
Effect of Angiotensin-Converting Enzyme Inhibition and Angiotensin II Receptor Blockers on Cardiac Angiotensin-Converting Enzyme 2
Carlos M. Ferrario , Jewell Jessup , Mark C. Chappell , David B. Averill , K. Bridget Brosnihan , E. Ann Tallant , Debra I. Diz , and Patricia E. Gallagher
Originally published16 May 2005https://doi.org/10.1161/CIRCULATIONAHA.104.510461Circulation. 2005;111:2605–2610
Competing interests: No competing interests