ABSTRACT
Vascular dysfunction results from arterial insufficiency and/or incompetence of the veno-occlusive mechanism (venous leak) (Brow et al., 2000). Differentiating between the two has prognostic and therapeutic implications (Table 7.4). Corporal fibrosis, which causes venogenic (venous leak) impotence, develops secondary to abnormalities in the regulation of collagen synthesis and degradation, probably related to chronic ischemia (Nehra et al., 1996). Erectile and sexual functions are regulated by dopamine and oxytocin release by the neurons of the hypothalamus. However, hypogonadism does not seem to contribute to the impaired penile reflex, as testosterone replacement does not cause the centrally mediated penile reflexes to recover (Sarapura and Schlaff, 1993; Sobrinho, 1993). Potassium (K) channels are key regulators of membrane potential and, therefore, of transmembrane Ca2+ flux, and, subsequently, the degree of contraction of many types of smooth muscle, including human corporal smooth muscle (Christ et al., 1995). Corporal smooth muscle tone, in turn, modulates penile blood flow
Table 7.1 Demographic distribution of erectile dysfunction
Country Age (years) ED (%)
USA 40-80 10-12 France 18-70 39 Spain 25-70 73 Nigeria 21-84 34 Korea > 50 59
and intracavernous pressure and, as such, affects both penile rigidity and erectile capacity. At least four subtypes of K channels are present in human corporal
myocytes, with the high conductance calcium-sensitive potassium channel (maxi-K or KCa channel) and the metabolically regulated potassium channel (KATP) being the most physiologically relevant. The low pO2 in patients with arteriogenic impotence, and the subset of men with severe venous leak impotence, support a concept of low cavernosal pO2 as a mechanism for both arteriogenic and venogenic impotence (Brow et al., 2000).
