In an experimental study (Wistar rats), it was found that pretreatment with atorvastatin increased the potency of sildenafil-induced relaxation (p < 0.01), the plasma NOx concentrations, and sildenafil-induced hypotension and tachycardia [41]. These findings suggest a synergy through NO-mediated mechanisms, in the vascular relaxation. In another study, atorvastatin ameliorated sildenafil-induced penile erections in spontaneously hypertensive rats, by interfering with the Rho-kinase signaling pathway within the penis [42]. Atorvastatin benefits on erectile function were also observed in diabetic rats and diabetic rabbits [43]. Similar beneficial effects on erectile function were also observed with rosuvastatin in obese diabetic rats [44]. Simvastatin showed similar benefits in restoring erectile function when added to insulin, by inhibiting the RhoA-/Rho-kinase pathway [45].

Case reports or small series of patients who were treated with gemfibrozil suggest that ED might appear after 1–3 weeks of treatment and subside after withdrawal of the drug [46–49]. A review of clinical trial experience with fenofibrate reported ED as an adverse effect on 1.3 % of the patients [50].

In a single-center prospective randomized placebo-controlled parallel-group trial of 160 male patients with ED and dyslipidemia, niacin was associated with improvement of erectile function compared to placebo for 12 weeks [51]. In another single-blind, one-arm study of 54 men with untreated ED, niacin had beneficial effects on erectile function when given combined with propionyl-L-carnitine and L-arginine for 3 months [52].

This review sought to summarize available evidence regarding the relationship between ED and dyslipidemia. Most evidence support that dyslipidemia is associated with ED through induction of impaired relaxation response upon cavernal tissue. Hypercholesterolemia decreases the gene expression of endothelium-specific cell-to-cell junction proteins and decreased endothelial content in the corpus cavernosum. High levels of ox-LDL induce lower bioavailability of NO.

Available data regarding the effects of statins on erectile function is conflicting. Experimental data point towards a beneficial effect of statins on erectile function through several mechanisms. Clinical data, however, does not confirm these beneficial effects in all cases. Available clinical studies show positive, neutral, or even negative effects on erectile function. However, existing data is not of the highest quality. Many studies are observational with all inherent limitations of this study type, and available prospective randomized studies have usually small study samples and short follow-up. Moreover, the assessment of erectile function in other studies was not based on validated methods. Finally, information regarding a dose-dependent effect or within-class differences are inconclusive.

Information regarding other hypolipidemic agents, apart from statins, is scant and fragmented. Gemfibrozil appears to have detrimental effects on erectile function, while niacin might beneficially affect erectile function; however, available data needs to be confirmed by appropriately designed and adequately powered clinical trials.