1. ¹Department of Urology, Haydarpasa Numune Training and Research Hospital, Bulgurlu mah. Uygarkent sit, Uskudar, Istanbul, Turkey
2. ²Department of Radiology, Vakif Gureba Training and Research Hospital, Bulgurlu mah. Uygarkent sit, Uskudar, Istanbul, Turkey

Correspondence: Dr C Kaya, Department of Urology, Haydarpasa Numune Training and Research Hospital, Bulgurlu mah. Uygarkent sit, A4 blok D17 Uskudar, Istanbul 81190, Turkey. E-mail: drckaya@hotmail.com

Received 3 June 2005; Revised 9 June 2005; Accepted 16 June 2005; Published online 28 July 2005.

Abstract

Erectile dysfunction (ED) and vascular disease are thought to be linked at the level of the endothelium. Endothelial dysfunction, resulting in the inability of the smooth muscle cells lining the arterioles to relax, prevents vasodilatation. Likewise, penile erection depends on the relaxation of smooth muscle in the corpus cavernosum and the wall of small arteries. The aim was to assess the systemic vascular function in patients with ED. In all, 32 ED patients diagnosed with Doppler Ultrasound and the International Index of Erectile Function-5-item questionnaire and 25 healthy men as a control group enrolled to the study. They all underwent the tests including serum glucose and lipid levels. Echocardiography and exercise stress test was performed routinely. Baseline demographics (body mass index, heart rate and blood pressures), fasting glucose and lipid levels were not significantly different between ED and control groups. Endothelial-dependent brachial artery flow-mediated vasodilatation and brachial artery response to 0.4 mg nitroglycerine (NTG) were measured. Participants were negative on exercise stress test, and echocardiographic parameters including ejection fraction were similar. Endothelial-dependent brachial artery percent diameter change with flow-mediated dilatation (6.012.9 vs 12.33.5) and brachial artery response to NTG (12.84.2 vs 17.85.2) were significantly different between groups (P<0.001). We found that endothelial function was impaired in ED patients with no apparent cardiovascular disease and diabetes mellitus. This impaired function might be explained by the abnormality in systemic nitric oxide–cyclic guanosine monophosphate vasodilator system and suggest that ED and vascular disease may be linked at the level of the endothelium.