The decrease in the expression of endothelial NOS and NOS activity in penile cavernous tissue caused by systemic inflammatory and oxidative stress status induced by exposure to PM<sub>2.5</sub> may be one of the important risk factors of erectile dysfunction.
Inflammatory and vascular parameters including myeloperoxidase (MPO), cyclooxygenase2 (COX2), endothelial nitric oxide synthase (eNOS), malondialdehyde (MDA), superoxide dismutase (SOD), reactive oxygen species (ROS), and cytokines in treated and untreated ED rats were measured.
The diabetic control group showed higher cGMP production level transcription and protein levels of eNOS and DKK3 and lower production levels of AGEs and miR-328 than the diabetic ED and diabetic ED+NC groups.
Gene therapy to the penile corpora cavernosa of cDNAs expressing PnNOS or eNOS, or counteracting PIN, has been effective in ameliorating ED in the aging rat model that exhibits both neurogenic ED and CVOD. cDNA constructs for other genes involved in the control of penile erection have also been successfully tested.
Previous studies demonstrated that cultured smooth muscle cells from corpus cavernosum display significantly altered K+ channel function, PGE-induced cAMP accumulation, and endothelin-1 induced Ca2+ mobilization that are consistent with the pathophysiology of erectile dysfunction.
To evaluate the protective role of bosentan (BOS), an endothelin-1 (ET-1) receptor antagonist, and to show the changes in rats with experimentally induced diabetic erectile dysfunction (ED), a total of 24 albino Wistar rats were allocated into four groups.
Higher levels of phosphorylated protein kinase B (p-AKT)/protein kinase B (AKT) (<i>p</i> < 0.05) and B-cell lymphoma-2 (Bcl-2) and lower levels of the apoptosis factors Bcl2-associated x (Bax) and caspase-3 were observed in the MSC-treated group than in the DM ED group (<i>p</i> < 0.05).
In addition, high stromal cell-derived factor-1 (SDF-1) expression was associated with increased vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in DM ED rats (<i>p</i> < 0.05).
The results showed that diabetes mellitus (odds ratio [OR] = 3.27, P < .01), hypertension (OR = 3.47, P < .01), and having the VEGF 2578A allele (OR = 1.54, P = .01) were the three most independent risk factors for ED.
We determined VEGF genotypes for three polymorphisms in VEGF promoter: -2578C>A (rs699947), -1154G>A (rs1570360) and -634G>C (rs2010963) in 126 patients with erectile dysfunction (ED; 66 patients with PED and 60 patients with CED).
The rat model of ED was established.Quantitative real-time PCR (qRT-PCR) and western blotting were used to detect the expression of lncRNA MIAT, von Willebrand factor (vWF), vascular endothelial cadherin (VE-cadherin), endothelial NO synthase (eNOS) and VEGF following BM-MSCs transfection.
Males with ED were older, and more prone to have a higher follicle-stimulating hormone, luteinizing hormone, sex hormone-binding globulin, glycated hemoglobin, fasting plasma glucose levels and lower free androgen index (FAI), UA levels, and more likely to have diabetes and elevated blood pressure compared with those without ED.
Among men with type 1 diabetes not using antihypertensive medications, higher SBP is associated with increased risk of developing erectile dysfunction.
Despite significant advances regarding ED pharmacological management, there are still insufficient responders to existing pharmacological treatments e.g., approximately 30% of patients are insufficient responders to phosphodiesterase type 5 inhibitors (PDE5-Is).
The objective of this study was to assess the cost-effectiveness of three separate phosphodiesterase type 5 (PDE5) inhibitors in ED therapy in a Norwegian setting.
Efficacy of treatment of ED in the CKD population is comparable to non-CKD patients across multiple modalities, including PDE5 inhibitors, vacuum erectile devices, intracavernosal injections and penile prostheses.
The success of sildenafil in the treatment of ED stimulated research in the field of PDE5 inhibition and led to many new applications, such as treatment of lower urinary symptoms, and pulmonary arterial hypertension, which are now approved indications.
Not only have phosphodiesterase-5 (PDE5) inhibitors improved the treatment of erectile dysfunction (ED), they have indirectly contributed to the treatment of male factor infertility.
Currently, PDE5 inhibitors (ex; Sildenafil, Tadalafil) available in the market are not only being used for the treatment of erectile dysfunction but at the same time, they are also in clinical trials being investigated as anticancer agents.
Therefore, the clinical management of ED related to aging can be done by therapeutic interventions that include PDE-5 inhibitors, and other pharmacological treatments.
In conclusion, our data showed no correlations of a novel polymorphism of the PDE5A promoter gene with the intermediate phenotype EH/ED and the BP and HR response to sildenafil administration.