The angiotensin-converting enzyme 2 (ACE2) receptor has been identified as the entry
receptor for the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that is abundantly
expressed in many organs. With respect to the role of circulating ACE2 and its receptor expression
in the pathogenesis of the SARS-CoV-2 infection, it is still debated whether diseases such as hypertension or pharmacotherapies, including ACE inhibitors and angiotensin receptor blockers that
affect ACE2 receptor expression, may modulate the severity and outcome of the coronavirus disease
2019 (COVID-19). We therefore tested the hypothesis that treatment with the ACE inhibitor Ramipril
affects organ-specific ACE2 receptor mRNA and protein expression as well as the serum metabolome
in BioBreeding (BB) rats. Twelve male BioBreeding rats were randomly divided into a Ramipril
(10 mg/kg body weight) treatment group or a control group (N = 12; n = 6 per group) over a
period of seven days. Ramipril treatment resulted in the reduction of acylcarnitines (C3–C6) out
of 64 metabolites. Among the different organs studied, only in the lungs did Ramipril treatment
significantly increase both Ace2 mRNA and ACE2 receptor membrane protein levels. Increased ACE2
receptor lung expression after Ramipril treatment was not associated with differences in ACE2 serum
concentrations between experimental groups. Our data provide experimental in vivo evidence that
the ACE inhibitor Ramipril selectively increases pulmonary ACE2 receptor mRNA and protein levels
and reduces acylcarnitines.
Identifer | oai:union.ndltd.org:DRESDEN/oai:qucosa:de:qucosa:85944 |
Date | 12 June 2023 |
Creators | Kosacka, Joanna, Berger, Claudia, Ceglarek, Uta, Hoffmann, Anne, Blüher, Matthias, Klöting, Nora |
Publisher | MDPI |
Source Sets | Hochschulschriftenserver (HSSS) der SLUB Dresden |
Language | English |
Detected Language | English |
Type | info:eu-repo/semantics/publishedVersion, doc-type:article, info:eu-repo/semantics/article, doc-type:Text |
Rights | info:eu-repo/semantics/openAccess |
Relation | 293 |
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