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Leptin plays a crucial role in blood pressure (BP) regulation, notably in the context of obesity through central sympatho-mediated pressor effects. Leptin also relaxes arteries via endothelial (EC) leptin receptor (LepR^EC)-mediated increases in nitric oxide (NO) bioavailability. Herein, we investigated whether leptin-mediated increases in NO bioavailability represent a buffering mechanism against leptin-induced sympatho-activation. We tested the direct contribution of LepR^EC to BP regulation in physiological conditions and in response to chronic leptin infusion using mice deficient in LepR^EC. LepR^EC deficiency did not alter baseline metabolic profile nor leptin-induced reduction in adiposity and increases in energy expenditure. LepR^EC−/− mice demonstrated no increase in baseline BP and heart rate (HR) (MAP: LepR^EC+/+:94.7 ± 1.6, LepR^EC−/−:95.1 ± 1.8 mmHg; HR:LepR^EC+/+:492.4 ± 11.7, LepR^EC−/−:509.5 …