The Epidemiology and Pathophysiology of Erectile Dysfunction

Abstract

Erectile dysfunction is a common condition associated with aging, chronic illnesses and various modifiable risk factors. Normal penile erection is a hemodynamic process that is dependent on corporal smooth muscle relaxation mediated by parasympathetic neurotransmission, nitric oxide, and possibly other regulatory factors and electrophysiological events. As more knowledge is gained of the physiology and regulatory factors that mediate normal erectile function, the mechanisms involved in the pathophysiology of erectile dysfunction should be further elucidated.

Sexual Symptoms in Endocrine Diseases: Psychosomatic Perspectives

“…However, most of evidence suggests that the androstenedione and T serum levels obtained from DHEA conversion do not result in sufficient androgenic effect [59]. Furthermore, it must be underlined that like thyroid diseases, adrenal diseases cause sexual disorders only in severe cases of adrenal hypo- or hyperactivity [60]. …”

Color Doppler imaging of erectile dysfunction: a new place in strategy?

“…A delicate balance is necessary between corporal smooth muscle contraction and relaxation to obtain a normal erection. If relaxation is deficient or contraction excessive, organic erectile dyfunction occurs [2]. Ultrastructural alterations of smooth muscle cells, as well as reduction in their number, could explain insufficient relaxation and expansion of the sinusoid spaces and a subsequent incomplete venous outflow compression allowing rigidity [3].…”

“…Contraction of smooth muscle cells is mediated by the sympathetic nervous system via norepinephrin synthesis, and peptides, such as endothelin 1, contribute to maintenance of their tone. Relaxation of smooth muscle cells is controlled by the parasympathetic nervous system via two neurotransmitters: acetylcholine first, then nitric oxide (NO), released by endothelial and efferent neuronal cells [2]. Nitric oxide induces the synthesis of cyclic guanosine monophosphate (cGMP) which is supposed to activate phosphorylation of proteins regulating corporeal smooth muscle tone, via the protein kinase G (the exact mechanism remains unknown).…”

“…In our experience, the number of penile Doppler studies has significantly decreased over the past 2 years. Con-2134 sidering the efficacy of available oral agents and the lack of proved efficacy of vascular surgical therapies in large populations, and knowing that the exact aetiological mechanisms responsible for abnormal erectile response have yet to be determined [2], the necessity to explore these patients has decreased; however, no consensus exists. Once neurological, hormonal, iatrogenic, and obvious psychogenic causes of erectile dysfunctions have been ruled out, vascular tests seem to be less mandatory than previously thought, as soon as an oral medication is accepted by the patient and is proved to be efficient.…”

Population pharmacokinetics and inter-laboratory variability of sildenafil and its metabolite after oral administration in Korean healthy male volunteers

“…[5,6] Malfunctions in this mechanism manifest as a reduction in NO release, leading to smooth muscle contraction and, eventually, to ED. [7] ED etiology includes organic and psychogenic mechanisms, [5] and organic etiology can be explained by malfunctions of the corpus cavernosum, which is controlled by NO release and cGMP stimulation. [7,8] Even though ED is a major cause of sexual dysfunction in males, [3] effective oral therapy for ED was not available until…”