Polycystic Ovarian Syndrome: Exploring Hypertension and Cardiometabolic Implications

Abstract

Polycystic ovarian syndrome (PCOS) is the most common endocrine disorder affecting women of reproductive age, with significant implications for cardiometabolic health. This review focuses on the relationship between PCOS and hypertension (HTN), an area that remains underexplored despite growing evidence of its importance. PCOS is characterized by hyperandrogenism (HA), ovulatory dysfunction, and polycystic ovarian morphology (PCOM), all of which contribute to a complex metabolic profile that includes insulin resistance (IR), obesity, and dyslipidemia. These factors collectively exacerbate the risk of HTN. Emerging research suggests HA in PCOS may directly influence the renin-angiotensin system (RAS), increasing blood pressure by promoting sodium retention and vascular tone. Additionally, IR, prevalent in both lean and obese women with PCOS, further contributes to HTN by enhancing sympathetic nervous system activity and impairing endothelial function. Despite these associations, the direct link between PCOS and HTN has not been definitively established, warranting further investigation. This review synthesizes current knowledge on the etiology of PCOS and its metabolic consequences, highlighting the need for targeted research to clarify the mechanisms linking PCOS with HTN. Understanding these pathways is crucial for improving the management of PCOS and reducing cardiovascular risks in affected women. By addressing these gaps, this review underscores the importance of considering HTN as a significant comorbidity in PCOS and calls for more comprehensive studies to guide clinical practice.