Rethinking the role of blood pressure drugs in COVID-19

Abstract

All it takes is a simple cough: a sharp intake of breath, the compression of air in the lungs, and the throat flying open to spew air, spit, and mucus If the person coughing is infected with the novel coronavirus, it comes along for the ride on droplets, which can travel up to 50 miles per hour When someone breathes those droplets in, the virus can get into the lungs Once inside, it uses a spike protein on its surface to target an enzyme—ACE2—scattered over the outsides of the airway’s cells If the spike protein connects with its target, the coronavirus uses ACE2 as a door to slip inside the cell Thus begins an infection During the early days of the coronavirus outbreak, researchers hypothesized that the likelihood of contracting COVID-19, the disease caused by the novel coronavirus, could be related to the amount of ACE2 on someone’s cells—the more doors for the virus to enter through, the higher the risk That idea prompted doctors around the world in March to warn the millions of people taking two classes of blood pressure medications, angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin II receptor blockers (ARBs), of a potential danger: these medications appear to increase ACE2 levels in cells, at least in some studies, so the drugs may make their users more susceptible to the novel coronavirus, SARS-CoV-2