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AGE RELTED ERECTILE DYSFUNCTION (ARED)

The interesting and stimulating talk was delivered by the eminent urologist,  Dr. Jacob Rajfer, Professor Emeritus at UCLA.

An abstract of his talk follows:

Prior to the 1980's there was no effective treatment for Male Erectile Dysfunction (ED). It was in the early 1990s that the PDE5 Inhibitors like Viagra, Levitra and Cialis revolutionized treatment for ED

Like any other species, humans are designed for the propagation of the species. The optimum age of fecundity is from puberty to the late twenties, when the degenerative process begins.

Oxidation, which is a byproduct of metabolism, affects the healthy functioning of the mitochondria in the smooth muscle cells. The resultant death and ultimate fibrosis of the cells, is a process known as APOPTOSIS.  Smooth muscle degenerative conditions include essential hypertension, gastro-esophageal reflux disease, over-active bladder, far-sightedness, constipation and the dreaded Erectile Dysfunction. The oxidative stress causes the degradation of the corporal cavernosal smooth muscle (CSM).

By the age of forty, a male has a 40% chance of having ED. The problem could be attaining and/or maintaining an erection long enough to complete the sexual act. This probability increases by 10% for every decade. So, if a person lives long enough, the occurrence of ED is inevitable. ED is influenced by other factors such as genetics, general health, life style choices like smoking etc.

The major reason of ED manifestation is an alteration in CSM of the penis. The CSM receives and traps blood entering the corporal bodies. The relaxation of the CSM creates sinusoidal spaces to fill with blood, and when an optimal intracorporeal pressure is reached, the veins draining the penis are closed off. Thus an erection is attained and maintained.

 There are multiple biochemical pathways involved in erection and dysfunction. Current drugs used to treat ED are only prescribed after ED is detected, and belong to a class called Type 5 phosphodiesterase (PDE5) inhibitors. These prevent the breakdown of cyclic guanosine monophosphate (cGMP), which is formed within the CSM from a reaction initiated by the Nitrous Oxide (NO), released from the Cavernosal nerve, through  the action of the enzyme n Nitrous Oxide Syntase (nNOS), present at the nerve endings,  following sexual stimulation. NO activates the enzyme Soluble Guanylyi Cyclase (sGC) in the cytoplasm of the CSM, thus converting Guanosine Triphosphate (GTP) into cGMP, which causes the relaxation of the smooth muscles and the increase of the intracavernosal volume. The endogenous PDE5 degrades cGMP, reversing the relaxation, causing penile flaccidity.

When the CSM cells are subjected to oxidation, the CSM induce an enzyme called inducible Nitric Oxide Syntase (iNOS), which produces NO in high quantities within the cells- NOT THE NERVE ENDINGS- to combat the oxidative stress . The NO produced at the nerve endings is only released after sexual stimulation, and is the major chemical involved in the relaxation of the CSM, thus initiating and maintaining erection.

Therefore, while nNOS is normally present in the nerves of the penis, iNOS is not normally present in the CSM, being induced only by the CSM cells when undergoing oxidative stress.

Whereas the PDE5 inhibitors are considered the first line of treatment of ED, they do come with notable side effects. Thus giving the PDE5 inhibitors on a regular basis may pose challenges in preventing the deterioration of ARED, which is characterized within the corpora by a progressive apoptosis of the smooth muscle cells and their replacement with collagen fibrous tissue. NO from iNOS has been shown to inhibit these histological changes in the corpora.

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