ERECTILE DYSFUNCTION EQUALS ENDOTHELIAL DYSFUNCTION ED=ED

Erectile dysfunction (ED) is defined as the consistent inability to obtain or maintain an erection for satisfactory sexual intercourse. ED was believed to be a psychological condition; however, in the past two decades, doctors have recognized that the majority of patients' erectile failure can be attributed to an organic cause. ED could result from neurologic, endocrine, or structural impairments. However, now research on erectile physiology has led to the conclusion that ED is predominately a disease of THE BLOOD VESSELS both arteries and veins and their unique penile structure, the corpus cavernosum (literally "cave-like bodies"). This is a pair of spongy tissues which if filled with blood, the penis becomes erect. The corpus cavernosum is composed of a meshwork of interconnected smooth muscle cells lined by vascular endothelium. The endothelial cells and underlying smooth muscle also line the small resistance helicine arteries that supply blood to the corpus cavernosum causing the organ to get hard (penile tumescence). Under stimulating circumstances, Nictric Oxide (NO) is released from the endothelium, a one cell thick lining, of the blood vessels. This causes relaxation of muscles around the arteries to the corpora cavernosa which engorges the penis with blood, increasing both its length and diameter. Blood can exit the erectile tissue only through a drainage system of veins around the outside wall of the corpus cavernosum. The expanding spongy tissue presses against the surrounding fibrous tissue, the tunica albuginea, constricting the veins, preventing blood from leaving. As a result, the penis becomes rigid .

Normal erectile function involves three synergistic and simultaneous processes: 1) neurologically mediated increase in penile arterial inflow, 2) relaxation of cavernosal smooth muscle, and 3) restriction of venous outflow from the penis.

Loss of the functional integrity of the endothelium and subsequent endothelial dysfunction plays an integral role in this issue. Pharmacological (Phosphodiesterase drugs such as Viagra) and endocrine (Testosterone) interventions help restore some function, but more is needed because of the 45% failure rate with these treatments. The incidence of ED dramatically increases in men who have endothelial dysfunction such as seen in middle age particularly those with diabetes mellitus, hypercholesterolemia, and cardiovascular disease. These diseases have in common a dysfunctional endothelium.

Penile erection is a psychoneurovascular phenomenon that depends upon cerebral stimulation, neural integrity, and a functional vascular system with healthy cavernosal tissues . It is the fit endothelium that produces the NO. Assuming the desire (libido), an intact nervous system and enough NO being produced from the endothelium, the penis will become erect and remain that way until it becomes refractory following ejaculation. Testosterone will encourage the brain if given sufficient visual and tactile clues. The intact nerves are needed not only for the brain to perceive touch, but to release the neurotransmitters to the penile arteries to dilate them. This dilatation to a large extent depends on the production of NO from the endothelium. If enough NO is released it will compensate for some lack of integrity of the neurovascularity. NO, then, is another therapy not generally used by doctors that is additive to testosterone and the phophodiesterase stimulators. Science has discovered several ways to increase NO production that will be discussed in another article.