Aim: 

Since endothelial dysfunction is thought to be the link between erectile dysfunction (ED) and coronary artery disease (CAD), the aim of this study was to evaluate the structural and functional changes of penile arteries (PA) and coronary arteries (CA) from insulin resistant Obese Zucker rats (OZR).

Methods: 

Branches of the dorsal penile artery (PA) and left descending coronary artery (CA) from OZR and control Lean Zucker rats (LZR) were mounted in microvascular myographs to evaluate vascular function. Both PA and CA were subjected to hematoxylin-eosin inmunostaining and western blotting to analyze eNOS expression.

Results: 

Internal diameter was reduced and wall-to-lumen ratio increased in PA from OZR. In contrast, structure was preserved in CA. Acetylcholine (ACh)-elicited relaxation was severely impaired in PA but not in CA from OZR although endothelial nitric oxide (NO) synthase expression was unaltered. Contractions to noradrenaline (NA) and 5-HT were significantly enhanced in both PA and CA from OZR. Blockade of NO synthase abolished endothelium-dependent relaxations in PA and CA, and potentiated NA and 5-HT contractions in arteries from LZR but not from OZR. The NO-mediated vasodilator response to the phosphodiesterase 5 (PDE5) inhibitor, sildenafil, was reduced in both PA and CA from OZR.

Conclusion: 

Whereas both structural alterations and impaired vascular reactivity are present in penile arteries from animals with Metabolic Syndrome, only a developing endothelial dysfunction is observed in coronary arteries. The severity of the altered structure and of the NO-mediated endothelial responses in PA might anticipate the functional impairment of the more preserved coronary vascular bed. Supported by grant SAF2006-09191