Novel nitric oxide signaling mechanisms regulate the erectile response

• Published in: International journal of impotence research Vol. 16; no. S1; pp. S15 - S19
• Main Author: Burnett, A L
• Format: Journal Article
• Language: English
• Published: England Nature Publishing Group 01.06.2004
• Subjects: Animals; Calcium - physiology; Erectile dysfunction; Homeostasis; Humans; Kinases; Male; Nitric oxide; Nitric Oxide - physiology; Nitric Oxide Synthase - physiology; Nitric Oxide Synthase Type I; Nitric Oxide Synthase Type III; Penile Erection - physiology; Penis; Penis - blood supply; Phosphorylation; Signal Transduction
• ISSN: 0955-9930; 1476-5489
• DOI: 10.1038/sj.ijir.3901209

Nitric oxide (NO) is a physiologic signal essential to penile erection, and disorders that reduce NO synthesis or release in the erectile tissue are commonly associated with erectile dysfunction. NO synthase (NOS) catalyzes production of NO from L-arginine. While both constitutively expressed neuronal NOS (nNOS) and endothelial NOS (eNOS) isoforms mediate penile erection, nNOS is widely perceived to predominate in this role. Demonstration that blood-flow-dependent generation of NO involves phosphorylative activation of penile eNOS challenges conventional understanding of NO-dependent erectile mechanisms. Regulation of erectile function may not be mediated exclusively by neurally derived NO: Blood-flow-induced fluid shear stress in the penile vasculature stimulates phosphatidyl-inositol 3-kinase to phosphorylate protein kinase B, which in turn phosphorylates eNOS to generate NO. Thus, nNOS may initiate cavernosal tissue relaxation, while activated eNOS may facilitate attainment and maintenance of full erection.