Related Experiment Video
Updated: Sep 26, 2025
08:35
Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion
Published on: May 26, 2022
3.5K
Ramipril Reduces Acylcarnitines and Distinctly Increases Angiotensin-Converting Enzyme 2 Expression in Lungs of Rats
Joanna Kosacka1,2, Claudia Berger1, Uta Ceglarek3
1Medical Department III-Endocrinology, Nephrology, Rheumatology, University of Leipzig Medical Center, Liebigstr. 20, 04103 Leipzig, Germany.
Metabolites
|April 21, 2022
Summary
The ACE inhibitor Ramipril increases lung ACE2 receptor expression and reduces specific acylcarnitines in rats. This study investigates Ramipril
Area of Science:
- Pharmacology
- Molecular Biology
- Metabolomics
Background:
- The angiotensin-converting enzyme 2 (ACE2) receptor is crucial for SARS-CoV-2 entry.
- The impact of ACE inhibitors on ACE2 expression and COVID-19 outcomes is debated.
Purpose of the Study:
- To investigate how Ramipril, an ACE inhibitor, affects organ-specific ACE2 expression and serum metabolome in rats.
- To test the hypothesis that Ramipril modulates ACE2 receptor expression.
Main Methods:
- BioBreeding rats were treated with Ramipril (10 mg/kg) or a control for seven days.
- Organ-specific ACE2 mRNA and protein levels were analyzed.
- Serum metabolome was assessed, focusing on 64 metabolites.
Main Results:
- Ramipril treatment significantly increased ACE2 mRNA and protein levels specifically in the lungs.
- A reduction in acylcarnitines (C3-C6) was observed among 64 measured metabolites.
- No significant difference in serum ACE2 concentrations was found between groups.
Conclusions:
- Ramipril selectively upregulates pulmonary ACE2 receptor expression in vivo.
- Ramipril treatment alters the serum metabolome by reducing specific acylcarnitines.
- Findings contribute to understanding ACE inhibitor effects in the context of viral infections.
More Related Videos
Related Concept Videos
01:30Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors
944
Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
944
01:26Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
539
The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
539
01:25Antihypertensive Drugs: Direct Renin Inhibitors
862
The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
862
01:30Antihypertensive Drugs: Angiotensin II Receptor Blockers
981
In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
981
01:18Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists
236
Endothelins (ETs) are potent vasoactive peptides critical in the human body's various physiological and pathological processes. One of the most promising therapeutic strategies for treating pulmonary arterial hypertension (PAH) involves counteracting the effects of these endothelins using a class of drugs known as endothelin receptor antagonists.
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme...
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme...
236