Downregulation of the expression of the P2Y1, P2Y2, P2Y4, and P2Y6 receptors that reduces the ratio of phosphorylated eNOS/eNOS and eNOS activity may be one of the important mechanisms of erectile dysfunction caused by low androgen status.
Electromagnetic cylinder ESWT device resulted in increased VEGF, nNOS, and eNOS expression; reduced smooth muscle atrophy; and increased endothelial cell regeneration in a DM-associated ED model.
Five genetic models and a generalized odds ratio (OR(G) ) were used to estimate the association between eNOSG894T and variable number of 27-bp tandem repeats in intron 4 (4 VNTR) and the risk of ED.
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.
In contrast, chronic alcohol administration changed the ultrastructures of the CC and suppressed eNOS expression, thereby leading to 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.
Our meta-analysis showed that the two single nucleotide polymorphisms in eNOS gene, G894T and T-786C, are strongly associated with the risk of erectile dysfunction.
Putative gene therapy interventions to restore eNOS expression and subsequent endothelial function may represent an exciting new therapeutic strategy for the future treatment of ED.
Several studies have focused on the impaired role of endothelial nitric oxide synthase (NOS3) gene polymorphism and its association to erectile dysfunction (ED).
The ec-NOS gene intron 4 VNTR, E298A and IVF 23+10 G/T polymorphisms were evaluated in the isolated DNA blood samples obtained from the patient group with ED (n=96), from the group received sildenafil (n=67) and from the healthy group (n=167).
The eNOS 894T allele carriers are at greater risk for both MtS and ED, suggesting that eNOS G894T gene polymorphism might play an implication as a common genetic susceptibility factor to develop both disorders.
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.
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.
The distributions of alleles (G894T, P < .005; T-786C, P < .015), genotypes (G894T, P < 0.015; T-786C, P < .010), and haplotypes (G894T/T-786C, P < .015) of the NOS3 polymorphisms were significantly different between patients with ED and controls.