Ignite Creation Date:
2025-12-24 @ 6:44 PM
Ignite Modification Date:
2025-12-25 @ 4:15 PM
Study NCT ID:
NCT05884957
Status:
COMPLETED
Last Update Posted:
2024-01-18
First Post:
2023-05-10
Is NOT Gene Therapy:
False
Has Adverse Events:
False
Brief Title:
Role of Nitric Oxide in Diabetic Patients With Erectile Dysfunction
Sponsor:
Egymedicalpedia
Organization:
Study Overview
Official Title:
Role of Nitric Oxide in Diabetic Patients With Erectile Dysfunction: Effect of Tadalafil Therapy
Status:
COMPLETED
Status Verified Date:
2024-01
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
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
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
Detailed 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
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
Study Oversight
Has Oversight DMC:
True
Is a FDA Regulated Drug?:
False
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?: