[Arterial hypertension in metabolic syndrome: pathophysiological aspects]

Area of Science:

• Cardiology
• Endocrinology
• Metabolic Disorders

Background:

• Arterial hypertension (AH) is a key component of metabolic syndrome.
• AH pathogenesis involves autonomic sympathetic dysfunction, hormonal axis activation, and endothelial dysfunction (ED).
• The condition is characterized by elevated blood pressure, left ventricular hypertrophy, and arterial remodeling.

Purpose of the Study:

• To elucidate the role of endothelial dysfunction and arterial remodeling in AH pathogenesis within metabolic syndrome.
• To explore the contribution of insulin resistance, hyperinsulinemia, and hyperleptinemia to AH development.

Main Methods:

• Review of existing literature on the pathophysiology of arterial hypertension and metabolic syndrome.
• Analysis of the mechanisms linking insulin resistance, hyperinsulinemia, and hyperleptinemia to sympathetic nervous system activity and blood pressure regulation.

Main Results:

• Endothelial dysfunction and arterial remodeling are central to AH pathogenesis in metabolic syndrome.
• Remodeling of resistant arteries increases peripheral resistance, stabilizing blood pressure.
• Remodeling of large arteries increases stiffness, leading to higher pulse and systolic blood pressure, and left ventricular hypertrophy.
• Insulin resistance and hyperinsulinemia activate the renin-angiotensin-aldosterone system, promoting AH, inflammation, and atherosclerosis.
• Hyperleptinemia stimulates sympathetic activity, contributing to elevated blood pressure in AH and obesity.

Conclusions:

• Endothelial dysfunction and arterial remodeling are critical drivers of arterial hypertension in metabolic syndrome.
• Hormonal and metabolic factors, including insulin resistance and hyperleptinemia, play significant roles in AH development and progression.
• Understanding these complex interactions is crucial for managing metabolic syndrome and preventing cardiovascular disease.