Anatomy, Physiology, and Pathophysiology of Erectile Dysfunction

Abstract

Introduction Significant scientific advances during the past 3 decades have deepened our understanding of the physiology and pathophysiology of penile erection. A critical evaluation of the current state of knowledge is essential to provide perspective for future research and development of new therapies. Aim To develop an evidence-based, state-of-the-art consensus report on the anatomy, physiology, and pathophysiology of erectile dysfunction (ED). Methods Consensus process over a period of 16 months, representing the opinions of 12 experts from seven countries. Main Outcome Measure Expert opinion was based on the grading of scientific and evidence-based medical literature, internal committee discussion, public presentation, and debate. Results ED occurs from multifaceted, complex mechanisms that can involve disruptions in neural, vascular, and hormonal signaling. Research on central neural regulation of penile erection is progressing rapidly with the identification of key neurotransmitters and the association of neural structures with both spinal and supraspinal pathways that regulate sexual function. In parallel to advances in cardiovascular physiology, the most extensive efforts in the physiology of penile erection have focused on elucidating mechanisms that regulate the functions of the endothelium and vascular smooth muscle of the corpus cavernosum. Major health concerns such as atherosclerosis, hyperlipidemia, hypertension, diabetes, and metabolic syndrome (MetS) have become well integrated into the investigation of ED. Conclusions Despite the efficacy of current therapies, they remain insufficient to address growing patient populations, such as those with diabetes and MetS. In addition, increasing awareness of the adverse side effects of commonly prescribed medications on sexual function provides a rationale for developing new treatment strategies that minimize the likelihood of causing sexual dysfunction. Many basic questions with regard to erectile function remain unanswered and further laboratory and clinical studies are necessary.

Sexual Dysfunction in Patients with Chronic Pain

“…This is strongly supported by the significant correlation between the VAS scores of pain intensity and severity of SD found in the present study. Another potential contributor to interference with normal sexual function is the use of medications such as antidepressants [21,22] and opioids [18,19,20,33]. In the present study, all four classes of medications (non-opioids, opioids, antidepressants and anticonvulsants) had been used in significantly higher percentages of patients with SD than by those who did not report SD.…”

Ca2+‐activated K+ channel (KCa) stimulation improves relaxant capacity of PDE5 inhibitors in human penile arteries and recovers the reduced efficacy of PDE5 inhibition in diabetic erectile dysfunction

“…Released from endothelia and nitrergic nerves, NO stimulates soluble guanylyl cyclase in smooth muscle, promoting cGMP generation. In turn, cGMP activates cGMPdependent protein kinase (cGK) which induces smooth muscle relaxation acting on different intracellular mediators (Gratzke et al, 2010). In addition, cGMP can directly act on specific ion channels in the cell membrane also facilitating relaxation of smooth muscle (Morgado et al, 2012).…”

137 Superparamagnetic Iron Oxide Nanoparticle Targeting of Adipose Tissue-Derived Stem Cells in Diabetes-Associated Erectile Dysfunction

“…26 However, under experimental hyperglycemic conditions, it has been demonstrated that oxidative stress contributes to neuronal, endothelial, and smooth muscle damage in diabetic animals. 23,27,28 In addition, in diabetic men, the smooth muscle and endothelial density in the corpus cavernosum is reduced significantly.…”