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Archivos Españoles de Urología (Ed. impresa)

versión impresa ISSN 0004-0614


MAS, Manuel. Molecular basis of erectile dysfunction. Arch. Esp. Urol. [online]. 2010, vol.63, n.8, pp.589-598. ISSN 0004-0614.

The penis physiological states of flaccidity or erection, result from the contraction or relaxation, respectively, of smooth muscle cells in the corpora cavernosa (CSMCs). They result from the interaction of various inter- and intracellular molecular signaling pathways. During the more usual state of flaccidity seems to predominate a tonic sympathetic activity, releasing nora-drenaline (NA) and other agonists that generate con-tractile signals in the CSMCs, with the likely cooperation of endothelium-derived messengers. Through activation of membrane receptors in the CSMCs they raise the in-tracellular messengers inositol triphosphate (IP3) and diacylglycerol (DAG). This results in a transient increase in cytosolic calcium concentration [Ca2+]i that starts the contractile response which is further sustained by the parallel agonist-induced activation of a "calcium sensitizing" mechanism involving the RhoA/Rho-kinase pathway. Overexpression of the latter might contribute to several vascular disorders as hypertension, vasospasm or erectile dysfunction. On sexual stimulation the cavernous nerves release nitric oxide (NO) that starts the erectile response. They also release acetylcholine that stimulates the endothelium to generate a more sustained release of NO. NO diffuses into CSMCs and increases their intracellular levels of cyclic guanosin monophosphate (cGMP) which decreases [Ca2+]i and deactivates the calcium sensitizing mechanism, thus relaxing CSMCs. This main physiological pathway for CSMCs relaxation is helped by the cyclic adenosin monophosphate (cAMP) pathway activated by various intercellular messengers from neural or paracrine sources, including prostaglandins E (PGE). Different phosphodiesterase enzymes (PDEs) inactivate the cyclic nucleotides thereby limiting their erectogenic action. Indeed the pharmacological inhibition of PDEs, especially the cGMP- specific PDE5, greatly enhances the erectile responses. There are cross-talk mechanisms between the cGMP and cAMP signaling pathways that offer additional possibilities for the pharmacotherapy of erectile dysfunction.

Palabras clave : Corpus cavernosum; Smooth muscle; Nitric Oxide; Cyclic nucleotides; Phosphodiesterases; Calcium sensitization; Erectile dysfunction.

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