Smooth muscle pathology and erection problems in older men

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Smooth muscle pathology and erection problems in older men

E Wespes of the Department of Urology, University of Charleroi, has written about the causes of erectile dysfunction as men age in the International Journal of Impotence Research, 2002, 14, supplement one pages 17 to 21. He begins by reviewing the mechanism of penile erection, stating that it is a complex phenomenon based both on neural and vascular physiology. Increased arterial flow has to be co-ordinated with smooth muscle relaxation of the sinusoidal spaces of the penis, and with decreased outflow of blood through the veins of the penis. Erection also involves the interaction of the brain, nervous system, neurotransmitters, and smooth and striated muscles. Clearly, in such a complicated system, any variation in the normal functioning of any one of these components has the potential to affect the erection response in the erectile tissue.

The Massachusetts Male ageing study has provided some data about the prevalence of erection problems as men age. Study of men between 40 and 70 years of age revealed that 52% of the sample had some degree of erection disorder. And indeed, erectile dysfunction is age-dependent: from 40 years of age to 70 years of age the probability of complete erectile failure trebles from 5% to 15%, while the probability of moderate erectile failure doubles from 17% to 34%. At the age of 70 only 32% of men describe themselves as completely free of erection problems.

Wespes asks whether erectile dysfunction can be explained by local structural changes in the penis. He used computerized analysis of images to show that the percentage of smooth muscle cells in men under 40 was 46% while by the age of 60 it was only 35%; he asks whether this reduction in smooth muscle content of the penis may be responsible for the increasing proportion of erectile problems in older men.

Turning to the veno-occlusive system, Wespes observed that the elasticity of the cavernosal tissue in the penis is essential to provide adequate compression on the veins leaving the penis so that their outflow is restricted. It is known that diabetes and hypercholesterolemia are both risk factors which interfere with the normal functioning of penile erectile tissue and can cause veno-occlusive failure. It is the percentage of smooth muscle content that determines whether or not venous leakage will occur in the penis of an older man. Men who have a low percentage of smooth muscle content have more difficulty maintaining an erection because blood can leak out of the penis more easily. In other words, the tunica albuginea is inflexible and fails to compress the veins so that blood is retained within the penis.

Wespes also asks what significance we can apply to changes in the elastic fibers or collagen of the penis. There are three types of collagen in the tissues of the corpus cavernosum, and it is believed that one particular type -- type III -- may decrease with age. This has been disputed in another study, but it's also possible that the collagen's chemical configurations may change with age so that overall, the effect is to reduce the number of elastic fibers in the penis.

And the third factor which decreases with age is the arterial inflow to the penis: the greatest decrease in blood flow into the penis was observed in men in the third and fourth decades of life, and it's highly probable that these alterations explain changes in erectile capacity of men as they age.

Wespes asks what might be responsible for these alterations in the biochemical structure of the penis. Post-mortem investigations have revealed that ageing has been associated with atherosclerotic vascular alteration of the arteries which feed the penis. In essence, it appears that the change is related to increasing fibrosis of the corpus cavernosum and associated blood vessels. A correlation between the level of oxygen in the penis and the percentage of smooth muscle fibers has also been demonstrated: this implies that the number of healthy muscular fibers in the penis is related to the capacity of the vascular system to supply adequate oxygenation to the penis. Deterioration of the arteries starts in the very small penile arteries as smooth muscle cells are replaced by fibrosis. As this process proceeds, a man will develop a corporeal veno-occlusive dysfunction which is later followed by severe arterial disease and major fibrosis of the corpus cavernosum.

Another role of adequate oxygenation in the corpus cavernosum appears to be the regulation of prostanoid production. Decreased levels of these prostaglandins correlate with the increased expression of the biochemical mechanism of fibrosis of the corpus cavernosum muscle cells; it's perhaps also not surprising that oxygen tension is significantly associated with nitric oxide synthesis, one of the major neurotransmitters responsible for erection. Low oxygen tension can potentially explain the decrease in the relaxation of smooth muscle fibers demonstrated in tissue culture studies. Indeed, the number of nitric oxide synthase containing fibers is reduced by half in old rats, and it may be that a reduction of these nerve fibers is the most important neurological factor in age-related erectile failure.

Role of testosterone in age related erection problems

Wespes goes on to speculate about the role of androgens in erectile response. Few close associations have been made between testosterone level and erectile capacity, and even when testosterone is supplemented in the ageing man, it often fails to restore erections to their previous level..

Studies have been conducted on various animal species about the consequences of castration and subsequent androgen replacement. It has been established that androgen receptors are present in the cavernosal tissue of most mammal species, and that androgen receptor activity varies widely with age, with the maximum level of activity occurring around about puberty, after which it declines significantly. This is an age-related change which is not reversible, and it's been speculated that the age-related decline in androgen receptors coincides with the end of penile growth. If, as is commonly believed, many androgens act primarily to stimulate or maintain the activity of nitric oxide synthase, then it follows that increasing levels of testosterone would have no impact on a man whose capacity to produce NOS had already declined.

A series of experiments has revealed that nitric oxide synthase enzyme protein reduces by 50% in castrated animals compared to those who've been castrated and received testosterone replacement. In adult rats, a decrease in NOS activity after castration can be restored with androgen replacement, although animals that had not been castrated who were given additional testosterone showed no extra NOS activity. Androgen dependence has been demonstrated for nerve stimulated intracavernosal pressures and corpus cavernosal smooth muscle integrity. Overall, these findings, which have been only partially represented here, and which are described in full in the original paper, suggest that androgen deprivation is responsible for functional and/or structural changes in the corpus cavernosum. In men who have normal levels of testosterone, supplementing testosterone does not increase the number of nocturnal erections, but it increases the rigidity of those erections, from which it has been inferred that testosterone acts on the cavernosal arterioles to control blood flow into the sinusoidal spaces.

Nocturnal erections reduce in older men and hypogonadal men: treatment with gonadotropin or testosterone does improve the quality of erection and nocturnal erection frequency. Wespes draws the conclusion that testosterone replacement is important for erections which occur during sleep but not for erections which occur in response to sexual fantasy or erotic visual stimulation.

In conclusion, Wespes asks how all this information can be used to improve or restore the intracavernosal structures to normality. He observes that prostaglandins seem to be able to suppress collagen synthesis in primary cultures of tissue cells, and so they may have the potential to prevent fibrotic lesions associated with erection problems and impotence. He further speculates that intracavernosal prostaglandin E1 injection might result in oxygenation of the corpora cavernosa and even some restoration of normal function of the connective tissue of the internal spaces of the penis. Sadly, however, people who have been treated with intracavernosal injection of prostaglandin E1 have not shown an increase in percentage of smooth muscle cells, which implies that any improvement in the erections of men treated with prostaglandin injections may be due to psychological or placebo effects rather than genuine changes in the structure of the penis. In conclusion Wespes observes that gene therapy might possibly represent one route to the restoration of normal erections in men who are suffering ED or complete impotence.

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