Résumé
Hyperinsulinemia has been classically associated with obesity-related hypertension. However, this concept has been challenged given that acute hyperinsulinemia has repeatedly failed to increase arterial pressure in humans. Most recently, leptin-dependent mechanisms have raised great interest as potential explanations for obesity-related hypertension. Despite potential depressor effects of leptin, most reports have shown that leptin increases arterial pressure probably due to sympathetic activation. Human obesity hypertension is associated with increased sympathetic activity. Thus, it is possible that hyperleptinemia in human obesity could contribute to obesity-related sympathetic activation. However, human obesity is a partial leptin resistant condition. The novel concept of selective leptin resistance may help explain leptin-induced sympathoactivation in obese subjects resistant to the metabolic effects of leptin. In this review article, we revisit insulin-dependent mechanisms reportedly associated with obesity hypertension. We also discuss leptin actions on the cardiovascular system and show experimental results that support the concept of selective leptin resistance.