Erectile dysfunction (ED) frequently coexists with coronary artery disease (CAD) and has been proposed as a potential marker for silent CAD in type 2 diabetes mellitus (DM). Since endothelial dysfunction is thought to be the link between ED and CAD, the purpose of the present study was to evaluate the functional responses of penile and coronary arteries from an animal model of Metabolic Syndrome. Branches of the dorsal penile artery (PA) and the left descending coronary artery (CA) from Zucker Lean (ZLR) and Zucker Fatty rats (ZFR) were mounted in microvascular myographs, and vasodilator and vasoconstrictor responses were recorded. Acetylcholine-elicited relaxations were severely impaired in PA from ZFR compared to ZLR (maximum response 33 ± 5% vs 79 ± 3%, n=20)and only slightly reduced in CA (pD2 6.72 ± 0.07 in ZFR vs 6.99 ± 0.08 in ZLR, n=22). Contractions to noradrenaline (147 ± 4 vs 179 ± 9% of KPSS in ZLR and ZFR, respectively, n=20) and 5–HT (114 ± 7% vs 165 ± 7%, n=22)were significantly enhanced in both PA and CA from ZFR. Blockade of NO synthase abolished endothelium-dependent relaxations in PA and CA, and potentiated noradrenaline and 5-HT contractions in arteries from ZLR but not from ZFR. The present results demonstrate a differential impairment of the NO-mediated endothelial responses of PA and CA in Metabolic Syndrome. The severity of the altered vasodilatation in PA might anticipate the functional impairment of the more preserved coronary vascular bed.

Supported by grants PR1/106-14441-A and SAF2006-09191.