Arterial hypertension (AH) is one of the basic components of metabolic syndrome that is caused by four factors: autonomic sympathetic dysfunction; activation of the hypothalamic-pituitary-adrenal axis; that of the renin-angiotensin-aldosterone system; and endothelial dysfunction (ED). AH is a slowly progressive hemodynamic disease, the natural course of which is characterized by not only elevated blood pressure (BP), but also by left ventricular hypertrophy, arterial remodeling, and a progressive increase in total peripheral resistance. ED and arterial remodeling play a key role in the pathogenesis of AH in metabolic syndrome. Remodeling of resistant arteries raises peripheral resistance and stabilizes BP and that of large arteries increases their stiffness and a reflected wave, resulting in increased pulse BP, systolic BP, and enhanced left ventricular hypertrophy. Insulin resistance and hyperinsulinemia increase the activity of the renin-angiotensin-aldosterone system and, by enhancing the expression of angiotensinogen, angiotensin II and its type 1 receptors, favors the development of AH, proinflammation, atherosclerosis, and congestive heart failure. Hyperleptinemia, which, by stimulating the activity of the sympathetic nervous system, elevates BP, plays a certain role in the development of AH in metabolic syndrome and obesity.