Description:
The angiotensin-converting enzyme 2 (ACE2) receptor has been identified as the entryreceptor for the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that is abundantlyexpressed in many organs. With respect to the role of circulating ACE2 and its receptor expressionin 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 thataffect ACE2 receptor expression, may modulate the severity and outcome of the coronavirus disease2019 (COVID-19). We therefore tested the hypothesis that treatment with the ACE inhibitor Ramiprilaffects organ-specific ACE2 receptor mRNA and protein expression as well as the serum metabolomein 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 aperiod of seven days. Ramipril treatment resulted in the reduction of acylcarnitines (C3–C6) outof 64 metabolites. Among the different organs studied, only in the lungs did Ramipril treatmentsignificantly increase both Ace2 mRNA and ACE2 receptor membrane protein levels. Increased ACE2receptor lung expression after Ramipril treatment was not associated with differences in ACE2 serumconcentrations between experimental groups. Our data provide experimental in vivo evidence thatthe ACE inhibitor Ramipril selectively increases pulmonary ACE2 receptor mRNA and protein levelsand reduces acylcarnitines.