Abstract
Erectile dysfunction is a disorder with a prevalence of up to 52% in men aged 40 years and above. About half of the affected men are not satisfied by the common treatment with phosphodiesterase type 5 inhibitors which inhibit cyclic guanosine monophosphate (cGMP) degradation. This low driven cGMP production could be attributable to comorbidities like diabetes. This study aims to investigate a new pharmacological mechanism, which enhances cGMP production independently of nitric oxide (NO). A total of 68 experiments were conducted on samples of human corpus cavernosum obtained from 12 men with erectile dysfunction who underwent penile implant surgery. The samples underwent ex vivo organ-bath assay and were exposed to one of the following three chemicals: soluble guanylyl cyclase stimulator (sGC-S; BAY 41-2272), soluble guanylyl cyclase activator (sGC-A; BAY 60-2270), or the control dimethylsulfoxide. When relaxation of the tissue occurred, the compound is more likely to generate an erection.
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