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DOI 10.1016/s0090-4295(02)01663-1

Медицинская библиотека · Urology · 2002

Type 5 phosphodiesterase expression in the human vagina.

D'Amati Giulia, di Gioia Cira R T, Bologna Mauro, Giordano Daniela, Giorgi Mauro, Dolci Susanna, Jannini Emmanuele A

СтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

OBJECTIVES

It has been demonstrated that clitoral and vaginal tissues express nitric oxide synthase isoforms in a way that parallels that of the penile corpus cavernosum. Considering the role of the vagina in the female sexual response and the anatomic connection between the clitoris and the anterosuperior vaginal wall, our aim was to study the distribution of type 5 phosphodiesterase (PDE5) in the anterosuperior wall of the human vagina.

METHODS

Immunohistochemistry was performed on the vaginal tissue of 14 women obtained at autopsy and on exfoliated cells of the vaginal epithelium obtained from 5 healthy female donors. Specific antibodies against PDE5 were tested on both paraffin sections and cytologic smears. Immunoblotting experiments were performed in parallel with the same antibodies.

RESULTS

The histologic analysis of human cadaveric vaginal tissue revealed that PDE5 immunoreactivity was mostly localized in the smooth muscle of vessels, forming a pseudocavernous tissue in the vaginal wall and endothelium. The Skene periurethral glands and vaginal epithelium were also positive for the antibody. The latter finding was confirmed using exfoliated cells of the vaginal epithelium harvested in vivo.

CONCLUSIONS

The presence and tissue distribution of PDE5 in the human vagina suggest that the integrated system of nitric oxide synthase-PDE5 may play a physiologic role not only in the male sexual response but also in female sexual arousal.

Для цитирования: D'Amati Giulia, di Gioia Cira R T, Bologna Mauro, Giordano Daniela, Giorgi Mauro, Dolci Susanna, Jannini Emmanuele A. Type 5 phosphodiesterase expression in the human vagina.. Urology. 2002. DOI: 10.1016/s0090-4295(02)01663-1.

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