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Erectile dysfunction in cyclic GMP-dependent kinase I-deficient mice.
Clinical Pharmacology, University of Lund, Lund, Sweden.
Experimental Pathology, University of Lund, Lund, Sweden.
Laboratory of Genetics, The Salk Institute, La Jolla, CA, USA.
Pathology, University of Lund, Lund, Sweden.
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2000 (Engelska)Ingår i: Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, E-ISSN 1091-6490, Vol. 97, nr 5, s. 2349-2354Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

The generation of nitric oxide (NO) in penile erectile tissue and the subsequent elevation of cyclic GMP (cGMP) levels are important for normal penile erection. Current treatments of erectile dysfunction elevate either cGMP levels by blocking cGMP degrading phosphodiesterase 5 or cyclic AMP (cAMP) levels by intrapenile injection of prostaglandin E1. The molecular target or targets of cGMP in erectile tissue and the role of cAMP for normal penile erection are not known. Herein, we report that mice lacking cGMP-dependent kinase I (cGKI) have a very low ability to reproduce and that their corpora cavernosa fail to relax on activation of the NO/cGMP signaling cascade. Elevation of cAMP by forskolin, however, induces similar relaxation in normal and cGKI-null corpus cavernosum. In addition, sperm derived from cGKI-null mice is normal, can undergo acrosomal reactions, and can efficiently fertilize eggs. Altogether, these data identify cGKI as the downstream target of cGMP in erectile tissue and provide evidence that cAMP signaling cannot compensate for the absence of the cGMP/cGKI signaling cascade in vivo.

Ort, förlag, år, upplaga, sidor
2000. Vol. 97, nr 5, s. 2349-2354
Nationell ämneskategori
Medicin och hälsovetenskap
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URN: urn:nbn:se:liu:diva-77621DOI: 10.1073/pnas.030419997PubMedID: 10688876OAI: oai:DiVA.org:liu-77621DiVA, id: diva2:528140
Tillgänglig från: 2012-05-24 Skapad: 2012-05-24 Senast uppdaterad: 2017-12-07

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