All the common risk factors for cardiovascular disease are associated with an enhanced oxidative stress and endothelial dysfunction. The production of superoxide is increased in these conditions and causes inactivation of NO. Cardiovascular risk factors increase the production of superoxide in endothelial cells where NO is produced causing immediate decrease in NO bioavailability, even when normal amounts are produced. Thus, the amount of bioactive NO is a function of the state of oxidative stress in the endothelium as much as of the total amount of NO synthesized by eNOS and in the situation of penile erection, also by bNOS. Mechanisms are not complete, however, because NO is not only released from endothe-lial cells but also from neurons in smooth muscle and possibly from the cavernous smooth muscle cells. So endo-thelial dysfunction, now proclaimed by many to be the root of the problem, may be only a branch (see Fig. 1).
In addition, the corpus cavernosum does not contain much muscle. Virtually all of the corpus cavernosum consists of a fine sponge-like framework whose interspaces communicate freely with one another and are filled with blood (Fig. 1). These spaces lead directly into veins of the penis. The size of the penis varies with the amount of blood in the erectile tissue, and there is more blood than muscle. Relaxation of muscle may not be as important a feature as stated in most descriptions of ED, and the use of phosphodiesterase inhibitors and the accumulation of cGMP causes a marked inflow of blood followed by entrapment of blood that maintains the erection.

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