Dysfonction érectile et cellules endothéliales caverneuses

Abstract

The physiopathology of erectile dysfunction (ED) is multifactorial. The recent discovery of the precise role of cavernosal endothelium in the functional regulation of the smooth muscle cells allowed to understand the physiological bases of erection. The purpose of this article is to make a synthesis of the current knowledge on the endothelial function and to allow a better understanding of the pathological responsible mechanisms of ED. Endothelium provides cavernosal smooth muscle cells relaxation by two main pathways: the NO/cGMP pathway induced by production of neural nitric oxide (NO) in cavernosal nerve terminals, and the AC/cAMP pathway which by-passes the NO route by using other mediators. This action allows the initiation and maintenance of erection. Risk factor-associated cavernosal endothelial alterations (diabetes mellitus, hypertension, hypercholesterolemia) are mostly induced by unifying mechanisms, including oxidative stress and accumulation of reactive oxygen species, alteration of NO production, or decrease of VEGF expression. The same cellular mechanisms can also be observed during aging. To a comprehensive appraisal of physiological bases of viable endothelium in erectile function, it is crucial to understand its biological activities. The hemodynamic evaluation of endothelial function and the current therapeutic implications will be later approached.