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Disfunzione erettile e Ossido Nitrico PDF Stampa E-mail
Monday 26 November 2007

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Akt-dependent phosphorylation of endothelial

nitric-oxide synthase mediates penile erection

K. Joseph Hurt*†, Biljana Musicki†‡, Michael A. Palese‡, Julie K. Crone‡, Robyn E. Becker‡, John L. Moriarity*,

Solomon H. Snyder*§¶, and Arthur L. Burnett‡

Departments of *Neuroscience, §Pharmacology and Molecular Sciences, ¶Psychiatry and Behavioral Sciences, and ‡Urology, Johns Hopkins University School

of Medicine, 725 North Wolfe Street, Baltimore, MD 21205

Contributed by Solomon H. Snyder, December 31, 2001

In the penis, nitric oxide (NO) can be formed by both neuronal NO

synthase and endothelial NOS (eNOS). eNOS is activated by viscous

dragshear stress in blood vessels to produce NO continuously, a

process mediated by the phosphatidylinositol 3-kinase (PI3-

kinase)Akt pathway. Here we show that PI3-kinaseAkt physiologically

mediates erection. Both electrical stimulation of the cavernous

nerve and direct intracavernosal injection of the vasorelaxant

drug papaverine cause rapid increases in phosphorylated

(activated) Akt and eNOS. Phosphorylation is diminished by wortmannin

and LY294002, inhibitors of PI3-kinase, the upstream

activator of Akt. The two drugs also reduce erection. Penile

erection elicited by papaverine is reduced profoundly in mice with

targeted deletion of eNOS. Our findings support a model in which

rapid, brief activation of neuronal NOS initiates the erectile process,

whereas PI3-kinaseAkt-dependent phosphorylation and activation

of eNOS leads to sustained NO production and maximal

erection.

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