Abstract
Obesity-associated arterial hypertension is characterized by stimulation of the sympathetic nervous system, activation of the renin-angiotensin system (RAS) and sodium retention, among other abnormalities. Stimulation of the sympathetic nervous system has been considered to have an important function in the pathogenesis of obesity-related hypertension. During the early phases of obesity, primary sodium retention exists as a result of increase in renal tubular reabsorption. Plasma renin activity, angiotensinogen, angiotensin II and aldosterone values display significant increase during obesity. Leptin and other neuropeptides are possible links between obesity and the development of hypertension. Obesity should be considered as a chronic medical condition, which is likely to require long-term treatment. Understanding of the mechanisms associated with obesity-related hypertension is essential for successful treatment strategies.
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