Pathophysiology
Clinical meaning
Erectile dysfunction (ED) results from failure of the penile vascular and neurological mechanisms required for erection. Normal erection requires parasympathetic nerve stimulation releasing nitric oxide (NO) from cavernous nerve terminals and endothelial cells. NO activates guanylate cyclase, increasing cyclic GMP (cGMP) in corporal smooth muscle, causing relaxation and allowing blood to fill the sinusoidal spaces of the corpora cavernosa. Phosphodiesterase-5 (PDE5) degrades cGMP, terminating the erection. ED may be vasculogenic (atherosclerosis, diabetes, hypertension affecting penile blood flow), neurogenic (diabetic neuropathy, spinal cord injury, radical prostatectomy), hormonal (hypogonadism, hyperprolactinemia), psychogenic, or medication-induced (antihypertensives, SSRIs, antiandrogens). ED is an independent cardiovascular risk marker - men with ED have a 2-fold increased risk of MI and stroke within 5 years.