Role of Nitric Oxide in Diabetic Patients With Erectile Dysfunction

Egymedicalpedia

Status: Completed

Conditions: Erectile Dysfunction; Diabetes Mellitus

Treatments: Diagnostic Test: Nitric oxide synthase gene

Study type: Interventional

Funder types: Industry

Identifiers

NCT05884957

Mona Hamza

Details and patient eligibility

About

Erectile dysfunction (ED) is defined as penile erection that is insufficient and unsustainable for a satisfactory sexual performance.

The etiology of ED is multifactorial including chronic diseases such as hypertension, diabetes mellitus and coronary artery disease However, the main underlying cause is degenerative changes that result in endothelial dysfunction

Full description

Diabetes leads to endothelial dysfunction and a pro-inflammatory state, which reduces the usability and activity of nitric oxide (NO). NO is a powerful force for sustaining penile blood flow.

Diabetes is an estab¬lished risk factor for sexual dysfunction in men; a three-fold increased risk of erectile dysfunction (ED) was documented in diabetics compared with non-diabetic men.

In smooth muscles, NO activates guanyl cyclase and increases cyclic guanosine monophosphate (cGMP) concentration. cGMP activates certain intracellular protein kinases that phosphorylate receptor proteins. Activated protein kinases open the potassium channels and increase the influx of potassium and block the influx of calcium by inhibiting calcium channels. This leads to hyperpolarization and relaxation of smooth muscle. Reduced arteriolar resistance leads to sinusoidal spaces filled with blood. These enlarged sinusoids further increase the intracavernosal pressure by blocking the venous return and producing a rigid erection. cGMP is converted to GMP by phosphodiesterase, which is inhibited by phosphodiesterase 5 (PDE-5) inhibitors.

(NO) has vasodilatory properties and balances RhoA/Rho-kinase-mediated vasoconstriction, which is a predominant mediator of the physiologic induction and maintenance of erections.

Evidences show that functional polymorphisms within endothelial NO synthase (eNOS) gene interfere with normal erectile function.

In humans, the eNOS gene is located on chromosome 7q35-36 and consists of 26 exons spanning 21 kilobases (kb). Several polymorphisms of eNOS have been investigated. More frequently, investigated regions of this gene include a variable number of 27 bp tandem repeats in intron 4 (VNTR), G894T (rs1799983) polymorphism in exon 7 and a T-786C (rs2070744) polymorphism in the promoter region

Enrollment: 40 patients

Sex: Male

Ages: 40 to 70 years old

Volunteers: Accepts Healthy Volunteers

Inclusion criteria

1. Diabetic patients with ED.
2. Using tadalafil 5mg

Exclusion criteria

1. Patients with history of pelvic trauma or major pelvic surgical intervention.
2. Patients with hypogonadism and hyperprolactinemia.
3. Patients with chronic liver disease or cardio vascular system diseases.
4. History of chronic intake of central nervous system, anti-androgen drugs or other drugs as Tramadol.
5. Smokers.
6. Patients with non-vasculogenic Erectile dysfunction

Trial design

Primary purpose: Treatment

Allocation: Randomized

Interventional model: Parallel Assignment

Masking: Triple Blind

---

40 participants in 2 patient groups, including a placebo group

Patients Group (Nitric oxide Assesment)

Active Comparator group

Description:

Assessment of nitric oxide synthase gene polymorphism in diabetic patients with erectile dysfunction in 30 patients

Treatment:

Diagnostic Test: Nitric oxide synthase gene

Control Group

Placebo Comparator group

Description:

10 healthy people without erectile dysfunction

Treatment:

Diagnostic Test: Nitric oxide synthase gene