Facteurs de risque cardiovasculaire, troubles de l’érection et dysfonction endothéliale

Cardiovascular risk factors, erection disorders and endothelium dysfunction

Pelvipharm SAS (Gif sur Yvette). E-mail : d.behr.roussel@pelvipliarm.com

Résumé

L’érection est un événement physiologique complexe qui, à la suite d’une stimulation sexuelle activant le système nerveux autonome, central et périphérique, fait intervenir plusieurs mécanismes endothélium-dépendants pour permettre la relaxation du muscle lisse des corps caverneux. La fonction endothéliale joue un rôle clé dans la physiologie locale de l’érection. La physiopathologie de l’insuffisance érectile (IE) suggère un lien étroit entre maladies cardiovasculaires et IE. Des données épidémiologiques et expérimentales concordantes suggèrent même que l’IE et la dysfonction endothéliale qui lui est souvent associée pourraient constituer un nouveau marqueur du risque cardiovasculaire. Ce concept devrait favoriser l’émergence de nouvelles stratégies thérapeutiques.

Abstract

Upon sexual stimulation, penile erection, occurring in response to the activation of pro-erectile autonomic pathways, is greatly dependent on adequate inflow of blood to the erectile tissue and requires coordinated arterial endothelium-dependent vasodilatation and sinusoidal endothelium-dependent corporal smooth muscle relaxation. Nitric oxide (NO) is the principal peripheral pro-erectile neurotransmitter which is released by both non-adrenergic, non-cholinergic neurons and the sinusoidal endothelium to relax corporal smooth muscle through the cGMP pathway. Any factors modifying the basal corporal tone, the arterial inflow of blood to the corpora, the synthe- sis/release of neurogenic or endothelial NO are prime suspects for being involved in the pathophysiology of erectile dysfunction (ED). In fact, conditions associated with altered endothelial function, such as ageing, hypertension, hypercholesterolemia and diabetes, may, by changing the balance between contractant and relaxant factors, cause circulatory and structural changes in penile tissues, resulting in arterial insufficiency and defect in smooth muscle relaxation and thus, ED. There is increasing evidence to suggest that ED is predominantly a vascular disease and may even be a marker for occult cardiovascular disease. Recent results illustrating the importance of endothelial dysfunction in the pathophysiology of different forms of experimental ED are discussed. These pathways may represent new potential treatment targets.