Pathophysiology of erectile dysfunction

Given the complexity of the system, it is not surprising that a wide variety of diverse disorders may result in erectile dysfunction (Table 1). Often, the cause is multifactorial, but vasculogenic causes are the most commonly implicated.

Vasculogenic Causes of ED
Neurogenic Causes of ED
Endocrinological Causes of ED
Priapism and Postpriapism ED
Psychogenic Causes of ED

Vasculogenic Causes of erectile dysfunction

Arterial insufficiency
Because the development and maintenance of a rigid erection depend on achieving a high intracavernosal pressure, it is not surprising that disorders affecting the peripheral arterial blood flow are strongly associated with erectile dysfunction (Table 2).

The most common cause is atheroma involving either the common or internal iliac arteries or their more distal branches (

Figure 28). The risk factors for this are similar to those for coronary artery disease (including smoking, hypertension, hyperlipidemia, diabetes mellitus and obesity). Narrowing or occlusion of the internal pudendal arteries reduces perfusion pressure to the corpora, resulting in a failure to achieve full rigidity. In the absence of such pressure, the normal veno-occlusive mechanisms cannot operate and, thus, the problem is compounded by secondary venous leakage. Obliterative disease of the aorta may also result in erectile dysfunction.

Venous leakage
In the presence of a normal arterial inflow, normal veno-occlusive mechanisms should slow egress of blood from the corpora to a virtual trickle during full erection. Failure to do so results in a flaccid erection and leakage of blood, either into the deep dorsal vein or the cavernosal venous system (

Figure 29). The etiology of this is obscure, but is more likely to be a primary disorder of intracavernosal smooth muscle than a problem primarily related to the penile veins themselves.


Table 1 Risk factors for erectile dysfunction

Vascular factors
  myocardial infarction
  coronary artery bypass surgery
  cerebral vascular accident
  peripheral vascular disease

Metabolic diseases
  diabetes mellitus
  renal failure
  chronic liver disease
  adrenal disorders

Neurological diseases
  multiple sclerosis
  multiple system atrophy
  Parkinson’s disease
  spinal cord injury

  acquired immunodeficiency syndrome (AIDS)


Table 2 Vascular pathophysiology of organic erectile dysfunction
Vascular etiology of erectile dysfunction present in 60% of patients. Small vessel vascular disease (e.g. diabetes) and large vessel arteriosclerosis (e.g. hypertension) cause arterial insufficiency/erectile dysfunction; erectile dysfunction occurs in 25% of men treated for hypertension and 60% of diabetics

Tobacco alters penile arterial hemodynamics, causing erectile dysfunction in a high proportion of elderly smokers; pelvic radiation leads to fibrosis/stenosis of pelvic arteries and accelerates existing arteriosclerosis; venous occlusive dysfunction may be due to decreased distensibility of corpora cavernosa or inherent abnormalities in tunica albuginea

Vascular endothelial growth factor may play a role in modulation of normal vascularity of penile architecture


Intracavernosal smooth muscle fibrosis

Full erection depends on achieving complete intracorporeal vasodilatation. This, in turn, depends on normally functioning corporeal smooth muscle. Aging and/or ischemia may result in degeneration of smooth muscle cells, thereby impairing the ability to respond to vasodilator signals. During flaccidity, the oxygen saturation of the blood within the lacunar spaces is low (40 mmHg). During erection, however, the inflow of arterial blood raises the oxygen saturation of lacunar blood to >90 mmHg.

The current evidence suggests that the development of intermittent erections may be an important mechanism for maintaining full oxygenation and, thus, function of cavernosal smooth muscle. Conditions of low oxygenation promote the production and release of transforming growth factor-β 1. This molecule, in turn, results in the formation of collagen, with the resultant development of intracorporeal fibrosis (

Figure 30). This may help to explain the physiological importance of the phenomenon of intermittent nocturnal penile tumescence. This is an important concept because it suggests that loss of erection due to any cause may be compounded by loss of cavernosal smooth muscle function and fibrosis. Clearly, such considerations may have an impact on the timing of treatment decisions in circumstances such as erectile dysfunction following radical prostatectomy.

Failure of intracavernosal neurotransmission
The molecular mechanisms of vasodilatation and vasoconstriction that underlie erection and detumescence have only recently been elucidated. Bearing in mind their complexity, it would be surprising if specific abnormalities of neurotransmission did not translate into clinical erectile dysfunction. As yet, however, none have been specifically described, but failure of NO production due to lack of NO synthase or abnormalities of receptor or second-messenger function may well underlie some cases. More research is needed in this rapidly evolving area.

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