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Here's WebMD's info on the subject which seems to implicate the corrective medication specifically rather than hypertension!:
https://www.webmd.com/lung/coronavirus-high-blood-pressure#1
Should a COVID-19 infected person immediately stop taking the inhibitor?
The article you linked to says
Another possibility is that the higher risk comes not from high blood pressure itself, but from certain drugs used to treat it -- ACE inhibitors and angiotensin receptor blockers (ARBs). This is just a theory, since there's no research yet on what impact, if any, these medications might have on COVID-19.
The theory is based on the fact that ACE inhibitors and ARBs raise levels of an enzyme called ACE2 in your body. And to infect cells, the COVID-19 virus must attach itself to ACE2.
Until more research comes out, the American College of Cardiology and American Heart Association recommend that you keep taking your high blood pressure medicine as prescribed. If you don’t, it could raise your risk for a heart attack or stroke, putting you in the hospital just as coronavirus cases are coming in.
Also (since that page doesn't have a clear date), there's an Apr 1 journal article that says
[...] we recently generated the hypothesis that these drugs might play a role in the severe course of COVID‐19 cases. More importantly, no clinical‐epidemiological data have been put forward and it is unknown whether the hypothesized mechanism plays a pivotal role in COVID‐19.
The lay press picked up the theory, causing concern and even anxiety among patients and their healthcare providers. Because of the lack of current evidence of a potential negative impact of these medications on COVID‐19, we currently support the position statement of the European and American Societies of Cardiology, who express that ACEIs and ARBs are safe and should be continued and prescribed according to established guidelines.
And a bit of "tune down" of their theory, now emphasizing/discussing the balance of effects (again, just theoretically, since no data has been apparently collected):
we cannot rule out that long‐term intake of ACEIs and/or ARBs may facilitate SARS‐CoV‐2 entry and virus replication. Conversely, it is yet unknown whether intake of ACEIs and/or ARBs, when infected, is beneficial with regard to pulmonary outcome. Possibly, we are dealing here with a double‐edged sword, depending on the phase of the disease: increased baseline ACE2 expression could potentially increase infectivity and ACEI/ARB use would be an addressable risk factor. Conversely, once infected, downregulation of ACE2 may be the hallmark of COVID‐19 progression. Consequently, upregulation by preferentially using renin‐angiotensin system blockade and ACE2 replacement in the acute respiratory syndrome phase may turn out to be beneficial.
Regardless of these deliberations, we would like to emphasize that many older patients are on renin‐angiotensin system blockade because of latent or manifest left ventricular dysfunction and that discontinuation of these drugs may exacerbate frank heart failure. There is little doubt that heart failure is prone to have an unfavorable effect on pulmonary outcome in the course of COVID‐19.
I don't think we really know if hypertension is truly an independent risk factor for disease severity in COvID-19. The first studies coming out of China indicated that hospital admissions listed hypertension as a co-morbidity factor in 70% or more of cases, but the prevalence of hypertension in the over 70 year olds is about 70% anyway. They then said the case fatality rate overall was 2.3% (among 44,672 cases) with those having hypertension being 6%, ie. nearly trebling the risk for severe disease.
However, hypertension is rarely a single disease and is usually associated with other morbidities such as ischemic heart disease, diabetes, renal disease, hyperlipidemia and gout. These are often under-diagnosed. It doesn't make biological sense that controlled hypertension itself would increase the case fatality rate. It was suggested that the use of ARBs and ACEI might increase the risk for disease severity but the observational data we now have suggests that ARBs reduce the risk to 34%, and there isn't enough data yet on whether ACEIs also have the same benefit.
https://jamanetwork.com/journals/jama/fullarticle/2762130
https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2764293
