Leptin is a peptide hormone secreted by white adipose tissue which is primarily involved in the regulation of food intake and energy expenditure. Recent studies suggest that leptin contributes to the pathogenesis of arterial hypertension associated with the metabolic syndrome. Plasma leptin concentration is increased in obese individuals. Moreover, chronic leptin administration or transgenic overexpression increases blood pressure in experimental animals, and some studies indicate that plasma leptin is elevated in hypertensive subjects independently of body weight. The purpose of this article is to characterize the relationship between leptin and vascular nitric oxide (NO), which plays a pivotal role in the regulation of blood pressure. Acutely administered leptin stimulates endothelial NO production, which counteracts simultaneous stimulation of the sympathetic nervous system and results in no net changes in blood pressure. Unfortunately, this acute NO-mimetic effect of leptin is impaired in obesity. This “vascular leptin resistance” may contribute to blood pressure elevation due to unopposed sympathetic activity. In addition, chronic hyperleptinemia may impair endothelial function by increasing formation of reactive oxygen species which scavenge NO. Recently, important progress has been made in understanding both the mechanism of resistance to acute NO-mimetic effect of leptin and unbeneficial impact of long-lasting hyperleptinemia on endothelial function.
Keywords: nitric oxide, endothelial dysfunction, obesity, arterial hypertension, oxidative stress
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