Abstract:
:In the penis, nitric oxide (NO) can be formed by both neuronal NO synthase and endothelial NOS (eNOS). eNOS is activated by viscous drag/shear stress in blood vessels to produce NO continuously, a process mediated by the phosphatidylinositol 3-kinase (PI3kinase)/Akt pathway. Here we show that PI3-kinase/Akt 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-kinase/Akt-dependent phosphorylation and activation of eNOS leads to sustained NO production and maximal erection.
journal_name
Proc Natl Acad Sci U S Aauthors
Hurt KJ,Musicki B,Palese MA,Crone JK,Becker RE,Moriarity JL,Snyder SH,Burnett ALdoi
10.1073/pnas.052712499keywords:
subject
Has Abstractpub_date
2002-03-19 00:00:00pages
4061-6issue
6eissn
0027-8424issn
1091-6490pii
99/6/4061journal_volume
99pub_type
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