What is Cyclic Guanosine Monophosphate (Cyclic GMP)?
Cyclic Guanosine Monophosphate (Cyclic GMP) is a guanine nucleotide containing a phosphate group esterified to the sugar moieties at the 3′ and 5′ positions. It is a cell regulator and has been described as a second messenger.
Its levels have been found to increase in response to various hormones such as acetylcholine, insulin and oxytocin, and activate specific protein kinases.
What is the role of nitric oxide in erectile dysfunction
Erectile dysfunction is a common multifactorial disorder associated with aging and various organic and psychogenic conditions such as hypertension, hypercholesterolemia, diabetes mellitus, cardiovascular disease, and depression.
Penile erection is a complex process involving psychogenic and hormonal inputs, and non-adrenergic and non-cholinergic neurovascular mechanisms.
Nitric oxide (NO) is the major non-adrenergic, non-cholinergic vasoactive neurotransmitter and is thought to be the chemical mediator of penile erection. NO released by neurons and endothelial cells in the corpus cavernosum activates soluble guanylate cyclase and increases levels of 3′,5′-Cyclic Guanosine Monophosphate (Cyclic GMP).
Acting as a second messenger molecule, cyclic guanosine monophosphate (Cyclic GMP) regulates the activity of calcium channels as well as intracellular contractile proteins that affect smooth muscle relaxation of the corpus cavernosum. The alteration of NO bioactivity is the main pathogenic mechanism of erectile dysfunction.
Treatment of erectile dysfunction often requires a combination of psychogenic and medical treatments, many of which have had only moderate success in the past.5) The advent of inhibitors has dramatically improved the treatment of erectile dysfunction.
Patients have shown high tolerance and success rates in improving erectile function. The efficacy of PDE-5 inhibitors also helps explain the importance of the NO-cGMP pathway in erectile function. Indeed, these agents interfere with the degradation of cGMP generated by NO.
Since not all patients respond to PDE-5 inhibitors, additional therapies that act on NO-independent and NO-dependent pathways, respectively, such as soluble guanylate cyclase activators and NO donors, are warranted. ‘Study.