Plasmatic renin-angiotensin system in normotensive and hypertensive patients hospitalized with COVID-19

• Published in: Biomedicine & pharmacotherapy 2022-08, Vol.152, p.113201-113201, Article 113201
• Main Authors: Silva, Mauro G., Corradi, Gerardo R., Pérez Duhalde, Juan I., Nuñez, Myriam, Cela, Eliana M., Gonzales Maglio, Daniel H., Brizzio, Ana, Salazar, Martin R., Espeche, Walter G., Gironacci, Mariela M.
• Format: Article
• Language: English
• Subjects: Adult; Angiotensin; Angiotensin II - metabolism; Angiotensin receptor blockers; Angiotensin-Converting Enzyme 2; Angiotensin-converting enzyme inhibitors; COVID-19; Humans; Hypertension; Peptidyl-Dipeptidase A - metabolism; Renin-Angiotensin System
• ISSN: 0753-3322; 1950-6007
• DOI: 10.1016/j.biopha.2022.113201

Besides its counterbalancing role of the renin-angiotensin system (RAS), angiotensin-converting enzyme (ACE) 2 is the receptor for the type 2 coronavirus that causes severe acute respiratory syndrome, the etiological agent of COVID-19. COVID-19 is associated with increased plasmatic ACE2 levels, although conflicting results have been reported regarding angiotensin (Ang) II and Ang-(1−7) levels. We investigated plasmatic ACE2 protein levels and enzymatic activity and Ang II and Ang-(1−7) levels in normotensive and hypertensive patients hospitalized with COVID-19 compared to healthy subjects. Ang II and Ang-(1−7), and ACE2 activity and protein levels were measured in 93 adults (58 % (n = 54) normotensive and 42 % (n = 39) hypertensive) hospitalized with COVID-19. Healthy, normotensive (n = 33) and hypertensive (n = 7) outpatient adults comprised the control group. COVID-19 patients displayed higher ACE2 enzymatic activity and protein levels than healthy subjects. Within the COVID-19 group, ACE2 activity and protein levels were not different between normotensive and hypertensive-treated patients, not even between COVID-19 hypertensive patients under RAS blockade treatment and those treated with other antihypertensive medications. Ang II and Ang-(1−7) levels significantly decreased in COVID-19 patients. When COVID-19 patients under RAS blockade treatment were excluded from the analysis, ACE2 activity and protein levels remained higher and Ang II and Ang-(1−7) levels lower in COVID-19 patients compared to healthy people. Our results support the involvement of RAS in COVID-19, even when patients under RAS blockade treatment were excluded. The increased circulating ACE2 suggest higher ACE2 expression and shedding. [Display omitted]