What are your thoughts on anti-hypertensive medications such as Losartan as far as how they could influence the severity of an infection?
Along the same lines, when we are told that high blood pressure is a risk factor, does that mean treated or untreated?
I have seen thoughts on both sides, some suggesting that because the virus binds to ACE2 as its means of entry into the body, that drugs which increase expression of that enzyme such as Losartan would lead to worse outcomes(which seems to be supported by the stats on hypertension as a comorbidity), but there are others saying that the increase in ACE2 has actually been shown to be protective and has been shown to prevent lung damage in other instances of viral pneumonia and ARDS, with some theorizing it could even be used as a treatment for covid19. But I'm not a doctor so I dont know what to think of it all since the info is so contradictory.
If your parents were on Losartan, would you have them continue taking it or try to switch to a calcium channel blocker or something else?
This is a great question.
Losartan is a angiotensin receptor blocker. It is somehow related to ACE inhibitors (which blocks conversion of angiotensin). Losartan may increase expression of the receptor (upgregulation) and upstream increase production of angiotensin 1 but as of now, there is insufficient data to say much about its effect on COVID expression or infection. HOWEVER, if you have high BP, it would make sense to switch to something like a CCB (norvasc or adalat)
Here's a paper published in the lancet: https://www.thelancet.com/pdfs/journals/lanres/PIIS2213-2600(20)30116-8.pdf
Thanks. That's the paper I was referring to.
But what about these contradictory points?
Upon reading this it appears that using ACE-i inhibitors they focused on a cardiac treatment.
These are generally taken orally. I wonder if there's some type of inhalant that would direct it to the lungs. This alone presents new risks.
There's also the soluble form of ACE2 that can be used to bind to the virus
Delivering excessive soluble form of ACE2.
Kuba et al.  demonstrated in mice that SARS-CoV downregulates ACE2 protein (but not ACE) by binding its spike protein, contributing to severe lung injury. This suggests that excessive ACE2 may competitively bind with SARS-CoV-2 not only to neutralize the virus but also rescue cellular ACE2 activity which negatively regulates the renin-angiotensin system (RAS) to protect the lung from injury [12, 30]. Indeed, enhanced ACE activity and decreased ACE2 availability contribute to lung injury during acid- and ventilator-induced lung injury [12, 31, 32]. Thus, treatment with a soluble form of ACE2 itself may exert dual functions: (1) slow viral entry into cells and hence viral spread [7, 9] and (2) protect the lung from injury [10, 12, 31, 32].