What is ED

Erectile Dysfunction Treatment

ED is the inability to achieve or sustain an erection suitable for sexual intercourse.

Penile erection is a complex physiologic process that occurs through a coordinated cascade of neurologic, vascular, and humoral events.

From an anatomic standpoint, the penis is highly vascular, invested with a rich supply of smooth muscle erectile tissue, and harbors numerous sinusoids, all of which render it well suited to accommodate the enhanced perfusion of the penis underlying physiologic erection.

Normal Erection Process for flaccid to erect  penis
Skin and vein treatment for ED erectile dysfunction

Penile erection is initiated by sexual stimuli, including auditory, visual, and olfactory stimuli, and erotic cognitions. Spinal cord sexual arousal occurs as a result of tactile stimulation of the penis.

Within the penis, erection begins with vasodilatation of the cavernous artery and helicine arterioles in association with relaxation of the trabecular erectile tissue. These actions cause engorgement of blood in the sinusoidal spaces of the corpora cavernosa and spongiosum, and penile erection results. The expansion of penile blood volume leads to compression of subtunicalvenules by the resistant fibrous outer covering, the tunica albuginea, with occlusion of venous outflow and physiologic erection.

The neurotransmitter mediating these sexual signals is nitric oxide (NO), initially termed endothelium-derived relaxing factor. NO is produced by the endothelium in the absence of cholinergic or adrenergic influences. NO stimulates smooth muscle guanylatecyclase, upregulating synthesis of cyclic guanine monophosphate (cGMP), which plays a pivotal role in penile arteriolar vasodilatation and relaxation of penile corporeal smooth muscle.

Oxygen levels are important in NO-mediated responses, which vary widely from penile flaccidity to erection. Decreasing oxygen tension levels progressively inhibit NO responses, and elevation of oxygen to normal levels restores NO-dependent activities.

Both cholinergic and adrenergic influences are significant in penile erection and detumescence. Parasympathetic fibers and acetylcholine, the release of which may be stimulated by tactile sensory stimuli to the penis, enhance penile blood flow and smooth muscle relaxation.[55] Sympathetic (adrenergic) fibers and norepinephrine neurotransmission help to maintain the penis in its flaccid state.

Detumescence is mediated by adrenergic nerve terminals whose neurotransmitter, norepinephrine, activates alpha-adrenergic receptors (found chiefly in the thoracolumbar region of the spinal cord). Activation of these receptors produces vasoconstriction of the penile vasculature and decompression of penile venules, which result in detumescence.

Incomplete corporeal smooth muscle relaxation resulting from impairment of the NO-induced relaxing mechanism or from augmented alpha-adrenergic activity has been proposed as a mechanism of ED.

Erectile Dysfunction Treatment
treatment of erectile dysfunction

Prostaglandin E1 (PGE1) is produced during erection by the penile musculature and activates adenylatecyclase, which alters ion-channel permeability and results in calcium release by the smooth muscle cells. (Although the PGE1 pathway is not thought to play a major intrinsic proerectile role, it is considered to be important as a therapeutic approach.)

These smooth muscle cells then relax, allowing increased blood flow. Dynamic vascular studies have demonstrated that venous outflow obstruction and the resultant entrapment of arterial blood in the penis are essential in the initiation and maintenance of a rigid erection.

Failure of these vascular phenomena, as seen with venous leakage, can result in ED.Venous leakage may be of traumatic origin, resulting in abnormal venous communication between the corpora cavernosa and the glans penis. Leakage may also result from the failure of emissary veins to close, as in Peyronie's disease.An unusual cause of ED is a traumatic or congenital arteriovenous fistula between the pudendal artery and a pelvic vein. An elevated penile content of corporeal connective tissue, possibly related to a decrease in oxygen, has been proposed as a mechanism for defective veno-occlusion.

Phosphodiesterases are essential in regulating intracellular cGMP activity through enzymatic hydrolysis (to 5'-GMP), thus terminating its second-messenger function. Multiple PDEs exist throughout the body; their isoforms vary depending on the specific function that they perform. In cGMP penile activity, the PDE5 isoform terminates the vasodilator and smooth muscle-relaxing effects of cGMP. Inhibition of this process by PDE5 inhibitors forms the basis for recent developments in the oral therapy of ED.

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