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Leptin induces relaxation of vascular smooth muscle through an endothelium-dependent release of nitric oxide (EDNO) and administration of a high-salt diet reduces the relaxation of vessels to EDNO. We would, therefore, predict that salt loading would reduce the leptin-induced dilatation. However, in salt-loaded animals the relaxation to acetylcholine is maintained through an endothelial-dependent hypopolarizing factor instead of EDNO. These experiments were, therefore, designed to examine whether in salt-loaded animals the response to leptin would be reduced or whether, as for acetylcholine, an alternative mechanism would be substituted.

Effects of dietary salt loading on the responses of isolated rat mesenteric arteries to leptin