Résumé : The increasing prevalence of obesity is largely responsible for the increase in related hypertension. These associated conditions are in turn leading to a dramatic increase in cardiovascular morbidity and mortality. Recent discoveries have underlined the active role of adipocytes in the occurrence of cardiovascular diseases through release of specific or non specific peptides. The latter are able to directly affect cardiovascular homeostasis and lead to hypertension. Possible mechanisms whereby obesity may contribute to hypertension include sympathetic activation, hyperleptinemia, insulin resistance, elevated angiotensin II and aldosterone levels, oxidative and inflammatory stress, endothelial dysfunction, impaired baroreflex function, and, perhaps, by effects on renal function. The management of this condition has never been validated by dedicated clinical trials and includes non pharmacological means (i.e. weight loss) as anti-hypertensive medications. Recent data show increased expression of angiotensin II–forming enzymes in adipose tissue, and increased activity of the renin-angiotensin system has recently been implicated in the development of insulin resistance and type 2 diabetes. Accordingly, antihypertensive agents that block the renin-angiotensin system might be beneficial for treatment of obesity-related hypertension. Both angiotensin-converting enzyme inhibitors and angiotensin type-1 receptor blockers have been associated with favourable metabolic properties and end-organ protection in addition to their antihypertensive effects. Data from ongoing large trials will provide an indication of the protective and preventive effects of these treatment strategies while offering insights into the mechanisms linking obesity, hypertension, and other facets of the metabolic syndrome.