Testosterone secreted from the Leydig cells of the testes under the influence of luteinizing hormone (LH) is necessary for normal male sexuality and sexual function (Table 4). Medications such as luteinizing hormone-releasing hormone (LHRH) agonists or stilbestrol, which lower circulating testosterone, result in loss of libido and in erectile dysfunction.
Patients who are hypogonadal as a result of pituitary or testicular dysfunction frequently suffer from erectile dysfunction, which responds to treatment with exogenous androgens. More contentious is the suggestion that waning testosterone levels in men of middle age and beyond (
Figure 32), the socalled ‘male menopause’, are a frequent cause of erectile dysfunction and, therefore, boosting serum testosterone levels has therapeutic benefits (Table 5).
However, there is some evidence from experimental animal models that androgens are necessary for the support of intracavernosal smooth muscle function and maintenance of NO synthase levels. Exogenous androgens are certainly capable of enhancing the libido, which is an important component of sexuality.
Dihydrotestosterone (DHT), the potent androgenic metabolite of testosterone produced by the enzyme 5α-reductase, is crucial for the normal development of the male external genitalia, seminal vesicles and prostate, but is not essential for either the libido or erectile function. Compounds such as finasteride, which inhibit the activity of 5α-reductase type II, result in shrinkage of the prostate by 20–30%, but have been reported to cause erectile dysfunction in only around 3–5% of patients.
However, in the 4-year placebo-controlled study of finasteride recently reported by McConnell and colleagues, nearly 14% of patients taking the active drug experienced some form of sexual dysfunction.
- Arterial Blood Supply
- Venous Drainage
- Lymphatic Drainage
- Central Nervous System Connections
- Causes of erectile dysfunction
- Vasculogenic Causes
- Neurogenic Causes
- Endocrinological Causes
- Priapism and Postpriapism ED
- Psychogenic Causes
- Risk factors for erectile dysfunction
- Diagnosis of erectile dysfunction Treatment of erectile dysfunction Erectile Dysfunction - Conclusions
Prolactin, which is released from the pituitary gland, acts as an inhibitory factor in male sexual function.
Hyperprolactinemia, either idiopathic or, less commonly, the result of a tumor such as a pituitary prolactinoma (
Figure 33), is associated with erectile dysfunction, as is the more common entity of idiopathic hyperprolactinemia. Correction of the raised prolactin levels using bromocriptine may sometimes restore potency in such patients.
Table 3 Neurogenic pathophysiology of organic erectile dysfunction
Diabetes, alcoholism/vitamin deficiencies contribute to somatic/autonomic neuropathy
Demyelinating diseases (e.g. multiple sclerosis) decrease penile sensation
Aging elevates sensory thresholds to vibratory/electrical stimulation
Pelvic/retroperitoneal surgery (e.g. radical prostatectomy) may damage the autonomic nervous system controlling the physiology of penile erection/ejaculation
Table 4 Endocrinological pathophysiology of organic erectile dysfunction
Low testosterone levels associated with decreased libido
Decline in nitric oxide synthase activity in castrated animals reversed by androgen supplementation
Nitric oxide synthase mRNA increases with androgen supplementation
Hypogonadism may be due to primary testicular failure, decreased secretion of gonadotropin releasing hormone (e.g. hyperprolactinemia), or alterations in steroid hormone protein binding (e.g. alcoholism, liver failure)
Table 5 Age-related pathophysiology of organic erectile dysfunction
Cellular senescence alters collagen content in corpora cavernosa/tunica albuginea, leading to venous occlusive dysfunction/decreased neuronal transmission to cavernosal smooth muscle
Aging alters endothelial function, leading to decreased basal nitric oxide release and up-regulation of basal endothelin-1
Reproductive aging in animals impairs neurogenic erectile response: increase in latency period to attain an erection/decrease in maximal intracavernosal pressure; loss of function integrity of endoluminal structures; imbalance in expression of vasoconstricting/vasorelaxing modulators of penile erection/decrease in nitric oxide synthase/increase in endothelin-1 levels