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Impaired nerve-mediated relaxation of penile tissue from caveolin-1 deficient mice.

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Author

Summary, in English

Caveolin-1-deficient mice are characterised by a high vascular NO production. Because NO-dependent smooth muscle relaxation is considered to play an important role in penile erection, it was hypothesized that the erectile function would be affected by genetic ablation of caveolae. This study assessed penile erectile mechanisms in caveolin-1 knockout (KO) mice ex vivo. Immunofluorescence confirmed caveolin-1 expression primarily in the endothelium surrounding the sinusoids of the corpus cavernosum, but also in smooth muscle cells of the sinusoidal bundles. In KO mice, caveolin-1 was absent, and the expression of the caveola-associated protein PTRF-Cavin was reduced. Nitric oxide synthase (endothelial and neuronal) and caveolin-3 levels were not affected, and staining of the neuronal marker PGP 9.5 did not disclose any apparent change in the density or pattern of innervation. Moreover, no apparent morphological differences were noted. Functionally, the force response following stimulation of alpha(1)-adrenergic receptors, and the sensitivity to the Rho-kinase inhibitor Y27632, were unaltered, whereas relaxation of alpha(1)-precontracted corpus cavernosum in response to electrical field stimulation and the muscarinic agonist carbachol were impaired. The nitric oxide donor sodium nitroprusside produced less relaxation in KO as compared to wild type corpus cavernosum. We conclude that nerve-mediated dilatation of the corpus cavernosum is impaired in the absence of caveolin-1, and that this is due in part to reduced sensitivity of the target tissue to NO. All in all our data support an important role of caveolin-1 in penile erection.

Publishing year

2009

Language

English

Pages

399-405

Publication/Series

European Journal of Pharmacology

Volume

602

Document type

Journal article

Publisher

Elsevier

Topic

  • Pharmacology and Toxicology

Status

Published

Research group

  • Vascular Physiology

ISBN/ISSN/Other

  • ISSN: 1879-0712