Abstract

ABSTRACT Endothelial dysfunction causes the failure of sildenafil response due to reduced nitric oxide (NO) . This study aimed to compare the biochemical and clinical effects of atorvastatin and vitamin E on endothelial function of sildenafil non‐responders with investigation to the underlying mechanisms.Methods: Sixty participants were randomly divided into three groups receiving atorvastatin 80 mg daily, or vitamin E 400 IU daily, or placebo capsules. Participants were examined both before and after six weeks for these biochemical tests; NO, glutathione peroxidase (GPO), interlukin 6 (IL‐6), testosterone, and endothelial nitric oxide synthase (eNOS) and for erectile function tests; international index of erectile function (IIEF ‐5) scores, rigiscan, and duplex l Results: in comparison to control group, the treated groups showed a significant increase in GPO, and a significant decrease in IL‐6. Atorvastatin only showed a significant increase in NO, eNOS, IIEF‐5 scores and rigiscan rigidity parameters. Other rigiscan parameters, testosterone and duplex ultrasound showed no difference in the three groups Conclusions: Atorvastatin improves endothelial function of sildenafil non‐responders by increasing NO level attributed to enhancing eNOS activity (main mechanism) added to antioxidant and anti‐inflammatory activities. Atorvastatin is a real promising drug for sildenafil non‐responders.

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