Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the human central nervous system. NO, ion channel, cytokine and testosterone play an important role in MS, and may be associated with the pathogenesis of ED. Meanwhile, the relationship between MS-induced peripheral nerve injury and ED should be understood correctly. Further researches on these mediators can provide some theoretical evidence for the clinical treatment of ED.
Erectile Dysfunction ; etiology ; metabolism ; Humans ; Male ; Multiple Sclerosis ; complications ; metabolism

The endothelium plays an important role in maintaining vascular homeostasis, regulating vascular tone and blood flow, and preserving a non-thrombogenic blood-tissue interface, and the normal function of the vascular endothelium is essential for penile erection. In most cases, erectile dysfunction (ED) is accompanied by endothelial dysfunction, and endothelial injury is a major pathological basis of ED, which can be induced by bad lifestyles, cardiovascular diseases, reactive oxygen species, and inflammatory mediators. The vascular endothelium is capable of self-repairing, and endothelial injury results from the unbalanced factors of injury and repair. This review focuses on the mechanism and repair of endothelial injury and the relationship of endothelial injury with ED.
Endothelium, Vascular ; metabolism ; pathology ; Erectile Dysfunction ; metabolism ; pathology ; Humans ; Male

Erectile dysfunction is a common complication of diabetes mellitus, and the pathogenesis of diabetic erectile dysfunction is very complicated, involving neuropathy, neurotransmitters, vasculopathy, vasoactive mediators, metabolism, endocrine and so on. Diabetes mellitus can cause oxidative stress, which plays an important role in the pathogenesis of diabetic complications. This review aims at the role of oxidative stress in the pathogenesis of diabetic erectile dysfunction.
Diabetes Complications ; metabolism ; Erectile Dysfunction ; etiology ; Humans ; Male ; Oxidative Stress

Microparticles are submicron vesicles shed from plasma membranes in response to cell activation, injury and/or apoptosis. Microparticles of various cellular origins, such as platelets, leukocytes, and endothelial cells, are found in the plasma of healthy subjects, and their amount increases under pathological conditions. Recent studies show that endothelial microparticles, a kind of envelope particles derived from endothelial cells, not only constitute a marker of endothelial dysfunction, but also play a major biological role in the diagnostic and therapeutic approaches to erectile dysfunction.
Biomarkers ; Cell Membrane ; Endothelial Cells ; metabolism ; pathology ; Erectile Dysfunction ; metabolism ; pathology ; Humans ; Liposomes ; metabolism ; Male

Erectile dysfunction (ED) is a common disease in men. Oxidative stress is indicated to be one of the important mechanisms of ED. NADPH oxidase expresses and plays significant psychological functions in many human organs, including the penis. In a variety of pathophysiological conditions, NADPH oxidase causes excessive oxidative stress through overproducing reactive oxygen species in the penis, and consequently induces erectile dysfunction. This paper reviews the composition, homologues, activation and physiological functions of NADPH oxidase, its role in ED, and its application in the treatment of ED.
Erectile Dysfunction ; enzymology ; therapy ; Humans ; Male ; NADPH Oxidases ; metabolism ; Oxidative Stress ; Reactive Oxygen Species

OBJECTIVETo study the impact of pulmonary fibrosis on erectile function in rats and its mechanism.

METHODSForty 12-week-old healthy male SD rats were randomly divided into Groups A (4-week pulmonary fibrosis), B (6-week pulmonary fibrosis), C (4-week control, and D (6-week control). The models of pulmonary fibrosis were established by injection of bleomycin at 5 mg/kg in the trachea, while the controls were injected with normal saline only. At 4 and 6 weeks, all the rats were subjected to determination of the serum testosterone (T) level, arterial blood gas analysis, measurement of intracavernous pressure/mean arterial pressure (ICP/MAP), and examination of NOS activity and cGMP content. The mRNA expressions of eNOS, iNOS and nNOS in the corpus cavernosum penis were detected by real-time PCR, and that of eNOS analyzed by Western blot.

RESULTSThe 3 V and 5 V of the ICP/mapx100 in Group C were 16.37 +/- 2.19 and 27.19 +/- 3.18, significantly lower than 30.78 +/- 2.66 and 50.09 +/- 6.97 in Group A (P < 0.05); those in Group D were 10.17 +/- 1.31 and 17.40 +/- 1.74, significantly lower than 31.45 +/- 3.07 and 51.23 +/- 7.23 in Group B (P < 0.05), and so were they in Group D than in C (P < 0.05). PaO2 was significantly lower in Group C than in A ([75.50 +/- 13.87] mmHg vs [103.80 +/- 6.88] mmHg, P < 0.05) , and so was it in Group D than in B ( [83.60 +/- 5.50] mmHg vs [102.70 +/- 5.77] mmHg, P < 0.05). Group C showed a significantly increased serum T level as compared with A ([391.1 +/- 264.7] ng/dl vs [175.9 +/- 53.0] ng/dl, P < 0.05), so did Group D ([745.4 +/- 408.8] ng/dl) versus Group B ([177.8 +/- 52.3] ng/dl) and C (P < 0.05). NOS activity and cGMP content in the corpus cavernosum significantly decreased in Group C ([1.50 +/- 0.14] U/mg prot and [35.69 +/- 3.64] pmol/mg) compared with A ([2.66 +/- 0.39] U/mg prot and [51.10 +/- 7.22] pmol/mg) (P < 0.05), so did they in D ([1.40 +/- 0.20] U/mg prot and [34.55 +/- 4.30] pmol/mg) versus B ([2.75 +/- 0.36] U/mg prot and [52.15 +/- 6.86] pmol/mg) (P < 0.05), but neither showed any significant difference between Groups D and C (P > 0.05). The expression of the eNOS protein was significantly lower in Group C than in A (0.79 +/- 0.01 vs 0.87 +/- 0.01, P < 0.05), so was it in D than in B and C (0.71 +/- 0.02 vs 0.88 +/- 0.01 and 0.79 +/- 0.01, P < 0.05). The expression of eNOS mRNA was significantly higher in Group C than in A (4.46 +/- 0.92 vs 2.61 +/- 0.68, P < 0.05), but did not show any significant difference between D and B (2.79 +/- 0.60 vs 2.69 +/- 0.65, P > 0.05), nor did the expressions of nNOS mRNA and iNOS mRNA between the pulmonary fibrosis groups and the controls (P > 0.05).

CONCLUSIONPulmonary fibrosis may induce erectile dysfunction by suppressing the expression of the eNOS protein and reducing NOS activity and cGMP content in the corpus cavernosum penis of rats.

Animals ; Erectile Dysfunction ; etiology ; metabolism ; Male ; Nitric Oxide Synthase ; metabolism ; Penis ; metabolism ; Pulmonary Fibrosis ; complications ; metabolism ; Rats ; Rats, Sprague-Dawley

Erectile function is a typical neurovascular process. Penile vascular endothelial dysfunction is indicated to be one of the important mechanisms of ED. Protective agents to improve penile vascular endothelial function show significant benefits to erectile function by decreasing the damage of oxidative stress and optimizing the related mediators. The protection of penile vascular endothelial function is a new approach to the treatment of ED.
Endothelium, Vascular ; metabolism ; Erectile Dysfunction ; therapy ; Humans ; Impotence, Vasculogenic ; metabolism ; physiopathology ; Male ; Oxidative Stress ; Penis ; blood supply

OBJECTIVETo investigate the changes of angiotensin II (Ang II) and its receptors in male rats with diabetic erectile dysfunction (DED) so as to study its effects.

METHODSOut of 40 male SD rats, 30 were taken at random for diabetic models. After 8 weeks, the rats with erectile dysfunction were selected from these models. All the rats were divided into 3 groups: control ( n = 10), diabetes mellitus( DM, n = 9) and DED (n = 8). For each rat, the Ang II levels in the blood and homogenate prepared from part of the isolated penile tissues were determined respectively, and the Ang II receptors of the rest of the penile tissues were analyzed through immunohistochemical (IHC) assay.

RESULTSCompared with the control group, Ang II levels in the blood and penile tissues in the DM group, and that in the blood of the DED group were very high and the differences were statistically significant (P < 0.05). Ang II in the penile tissues of the DED increased sharply (P < 0.01). The receptors of Ang II changed contrariwise to the level of Ang ll.

CONCLUSIONAng II may play an important role in the pathogenesis of DED, and the Ang II antagonist or inhibitor of the angiotensin-converting enzyme (ACEI) may become a therapeutic method for DED in the future.

Angiotensin II ; blood ; metabolism ; Animals ; Diabetes Complications ; blood ; metabolism ; Erectile Dysfunction ; blood ; etiology ; metabolism ; Immunohistochemistry ; Male ; Penis ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Receptors, Angiotensin ; blood ; metabolism

OBJECTIVETo investigate the role of endogenous hydrogen sulfide (H2S) in erectile dysfunction (ED) induced by androgen deficiency.

METHODSWe randomly divided 30 eight-week-old healthy male SD rats into six groups: 2-week control (A), 4-week control (B), 2-week castration (C), 4-week castration (D), 2-week castration + androgen replacement (E), and 4-week castration + androgen replacement (F), those in groups E and F subcutaneously injected with testosterone propionate (TP) at the physiological dose of 3 mg/kg per day after castration, while those in the other groups with isodose oil instead. At 2 and 4 weeks after operation, we determined the level of serum testosterone (T) , intracavernous pressure (ICP) , mean carotid arterial pressure (MAP) of the rats, measured the concentration of H2S in the plasma and corpus cavernosum tissue, and detected the expressions of cystathionine-P3-synthase (CBS) and cystathionine-gamma-lyase (CSE) by immunohistochemistry and Western blot.

RESULTSThe serum T level was significantly lower in group C ([0.63 +/- 0.15] nmol/L) than in A ( [ 16.55 +/- 4.17] nmol/L) and E ( [ 18.99 +/- 4.62] nmol/L) (P <0.05), as well as in group D ([0.70 +/-0.22] nmol/L) than in B ([15.44 +/-5.18] nmol/L) and F ([20.99 +/-6.41] nmol/L) (P <0. 05) , and so were ICP/MAP after 5 and 7 V electrical stimulation of the pelvic ganglia (P <0. 05) , H2 S concentration (P <0.05), and the expressions of CBS and CSE (P <0.05). The expressions of CBS and CSE proteins were also significantly decreased in group C as compared with D (P <0.05).

CONCLUSIONThe reduced expressions of CBS and CSE may inhibit the H2 S signaling pathway, which might be one of the mechanisms underlying androgen deficiency-induced ED in rats.

Androgens ; deficiency ; Animals ; Cystathionine beta-Synthase ; metabolism ; Cystathionine gamma-Lyase ; metabolism ; Erectile Dysfunction ; metabolism ; Hydrogen Sulfide ; metabolism ; Male ; Orchiectomy ; Penis ; metabolism ; Rats ; Rats, Sprague-Dawley

Erectile dysfunction (ED) is an almost unavoidable complication of radical prostatectomy. At present, though the concept of penile rehabilitation (PR) is accepted by most clinicians, the outcomes of erectile function recovery vary widely. Prostacyclin (PGI2) is a prostanoid and a main vasoprotectant which induces smooth muscle relaxation, but not used for replacement therapy because of its high unstability. SuperEnzyme is capable of continuous, specific and targeted promotion of PGI2 synthesis, and helps PR in ED patients after radical prostatectomy. SuperEnzyme gene therapy has a promising prospect for PR and the management of ED. This review updates SuperEnzyme gene therapy in PR.
Enzyme Therapy ; Epoprostenol ; Erectile Dysfunction ; rehabilitation ; therapy ; Genetic Therapy ; methods ; Humans ; Male ; Penile Erection ; Penis ; Prostaglandin-Endoperoxide Synthases ; metabolism