<p>Changes in the relative contribution of endothelium-produced vasodilators to the modulation of mesenteric artery reactivity were studied in Wistar rats treated with 20% fructose for 16 and 32 weeks. Rats that consumed fructose developed symptoms of metabolic syndrome. Acetylcholine-induced relaxation of phenylephrine-precontracted mesenteric arteries was reduced in rats with metabolic syndrome. The NO-mediated component of acetylcholine-induced relaxation was reduced in these rats. At the same time, arterial relaxation mediated by endothelium-dependent hyperpolarization was increased. Endothelium-independent relaxation of mesenteric arteries to sodium nitroprusside in rats with metabolic syndrome was the same as in the arteries of control rats. These results suggest that the increased contraction of mesenteric arteries caused by phenylephrine in rats with metabolic syndrome is due to decreased NO production by the endothelium. Endothelium-dependent hyperpolarization appears to partially compensates for this dysfunction.</p>