Leptin Causes Vasodilation in Humans

Abstract

P177 Background: Recently, it was reported that the acute infusion of the leptin markedly increased sympathetic nerve activity, but did not change arterial pressure, and it was also reported that the leptin receptor was expressed in human endothelium. Therefore, we suggested that the leptin might induce the vasodilation that counterregulate vasoconstricting response which is induced by sympathetic activation. Methods: To evaluate the effect of the leptin on forearm circulation, we measured the forearm blood flow(FBF)response to intra-arterial infusion of the human recombinant leptin(1, 10, 100 ng/kg/min, for 5 minutes, respectively) in seven healthy male subjects (age 23.3±1.7 years). FBF was measured using venous occlusion plethysmography. Results: The leptin infusion significantly increased the FBF in the dose-dependent manner (5.9±2.2%, 13.9±3.0%, 14.4±3.6%, at each doses, p<0.05). The intraarterial infusion of NG-monomethyl-L-arginine (L-NMMA), a nitric oxide synthese inhibitor, did not alter FBF response to the leptin (3.3±4.2%, 21.2±9.7%, 15.5±3.7%, at each doses, p<0.05). No significant changes in blood pressure or heart rate were detected during the infusion of leptin, and leptin in conbination with L-NMMA in all subjects. Conclusion: These findings suggest that the leptin per se directly causes the vasodilatation, and that leptin-induced vasodilatation is not due to the increase in nitric oxide production in healthy subjects.