Angiotensin-Converting Enzyme Inhibitors and Adipokines: The Role of Visfatin and Apelin in Cardiovascular Disease Management
Abstract
Background: Angiotensin-converting enzyme (ACE) Inhibitors are medications pivotal in cardiovascular disease management, impacting the renin-angiotensin system which plays a critical role in cardiovascular health. These inhibitors not only modulate blood pressure and fluid balance but also influence adipose-derived hormones like visfatin and apelin. These adipokines are intricately linked with cardiovascular function and interact with the renin-angiotensin system, thereby affecting cardiovascular disease outcomes. Understanding the interplay between ACE inhibitors, visfatin, and apelin is crucial for optimizing therapeutic strategies in cardiovascular disease management. Visfatin is primarily expressed in visceral adipose tissue and is associated with hypertension, vascular inflammation, and insulin resistance. Elevated serum levels of visfatin correlate with increased systolic and diastolic blood pressure. Apelin, acting through the G protein-coupled receptor APJ, is implicated in cardiac system diseases and can lower arterial blood pressure, improving cardiac output. Different apelin isoforms have varying efficacies in arterial pressure regulation. ACE inhibitors, widely prescribed for hypertension and heart failure, are found to modulate serum levels of apelin and visfatin, potentially augmenting their cardioprotective effects. Aim: This review article aims to elucidate the effects of angiotensin-converting enzyme (ACE) inhibitors on the serum levels of visfatin and apelin and their implications for cardiovascular disease management. Conclusion: The interactions between ACE inhibitors, visfatin, and apelin present promising avenues for targeted therapies in hypertension and cardiovascular diseases. Despite some inconsistencies in the research, understanding these interactions could lead to novel therapeutic approaches and enhanced cardiovascular care.
References
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