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En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries
Published on: February 25, 2016
Polymorphism of endothelial nitric oxide synthase gene in patients with erectile dysfunction
Erkan Erkan1, Ahmet Yaser Muslumanoglu, Tayfun Oktar
1Department of Urology, Haseki Teaching and Research Hospital, Istanbul, Turkey. ilhanerkan@yahoo.co.uk
Introduction:
Endothelial-derived nitric oxide (NO), which is produced by endothelial nitric oxide synthase (eNOS) in response to increased blood flow, maintains the tumescence phase of erection. The eNOS gene is located on the seventh somatic chromosome and the polymorphism of this gene has been reported to cause changes in the structure of enzyme system, resulting in disturbance of its activity.
Aim:
The aim of this prospective study is to evaluate the relationship between polymorphism of eNOS gene and erectile dysfunction (ED).
Methods:
Thirty patients with ED (mean age: 58.7 +/- 9.97, range: 39-74 years) and 25 voluntary controls (mean age: 56.44 +/- 7.58, range: 47-72 years) were enrolled to the study. Patients with ED were evaluated with International Index of Erectile Function (IIEF) questionnaire, routine blood tests for systemic vascular risk factors, and color Doppler ultrasonography while potency of the control group were only assessed with IIEF questionnaire. The presence of polymorphism of eNOS gene was determined in both groups by polymerase chain reaction in the fourth intron of the seventh somatic chromosome that encodes eNOS gene.
Results:
The incidences of diabetes mellitus and coronary artery disease were statistically higher in the ED group (P = 0.023 and 0.029, respectively) while mean IIEF score was significantly lower (P = 0.001). Evaluation with color Doppler ultrasonography revealed penile arterial insufficiency in six cases, cavernosal insufficiency in 19 cases, and mixed vascular insufficiency in five cases. The distributions of three eNOS genotypes (eNOS4b/b, eNOS4a/b, and eNOS4a/a) among ED patients and controls were similar (P > 0.05). However, eNOS4a/b genotype was statistically higher in diabetics (P = 0.042). Also, 80% of the patients with severe ED and 54.5% of the diabetic patients with ED had eNOS4a/b genotype.
Conclusion:
In our study, no correlation was detected between the polymorphism of eNOS gene and ED. However, 80% of the patients with severe ED and 54.5% of the diabetic patients with ED had eNOS4a/b genotype. Based on our data, it seems that diabetic patients with ED tend to have more eNOS4a/b genotype.
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