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    Proc Natl Acad Sci U S A. 2006 Feb 28;103(9):3440-3. Epub 2006 Feb 17.

    Alternatively spliced neuronal nitric oxide synthase mediates penile erection.

    Hurt KJ, Sezen SF, Champion HC, Crone JK, Palese MA, Huang PL, Sawa A, Luo X, Musicki B, Snyder SH, Burnett AL.

    Source

    Department of Urology, Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

    Abstract

    A key role for nitric oxide (NO) in penile erection is well established, but the relative roles of the neuronal NO synthase (nNOS) versus endothelial forms of NOS are not clear. nNOS- and endothelial NOS-deficient mice maintain erectile function and reproductive capacity, questioning the importance of NO. Alternatively, residual NO produced by shorter transcripts in the nNOS(-/-) animals might suffice for normal physiologic function. We show that the beta splice variant of nNOS elicits normal erection despite a decrease in stimulus-response characteristics and a 5-fold increased sensitivity to the NOS inhibitor, l-NAME. Residual nNOSbeta generates only 10% of the normal NO level in vitro but produces citrulline and diaphorase staining reflecting in vivo NOS activity in pelvic ganglion nerves that is comparable to WT animals. Thus, alternatively spliced forms of nNOS are major mediators of penile erection and so may be targets for therapeutic intervention.

    PMID:
    16488973
    [PubMed - indexed for MEDLINE]
    PMCID: PMC1413936
    Free PMC Article

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