alexa Nitric Oxide Synthase is Necessary for Normal Urogenital Development
ISSN: 2167-0250

Andrology-Open Access
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Research Article

Nitric Oxide Synthase is Necessary for Normal Urogenital Development

Christopher Bond1, Omer Onur Cakir1, Kevin T McVary2 and Carol A Podlasek1*
1Department of Urology, Northwestern University, Feinberg School of Medicine, Chicago, IL, USA
2Division of Urology, Southern Illinois University School of Medicine, Springfield, IL, USA
*Corresponding Author : Carol Podlasek
PhD, Department of Urology
Northwestern University
303 E. Chicago Avenue, Tarry 16-763
Chicago, IL 60611, USA
Tel: +312-503-7247
Fax: 312-908-7275
E-mail: [email protected]
Received September 05, 2013; Accepted October 29, 2013; Published November 04, 2013
Citation: Bond C, Cakir OO, McVary KT, Podlasek CA (2013) Nitric Oxide Synthase is Necessary for Normal Urogenital Development. Andrology 2:108. doi:10.4172/2167-0250.1000108
Copyright: © 2013 Bond C, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Introduction: Neuronal nitric oxide synthase (NOS-I) is significantly decreased with Cavernous Nerve (CN) injury in Erectile Dysfunction (ED) models. Increased apoptosis and collagen deposition accompany decreased NOS/CN injury, however these changes are typically attributed to the altered signaling of other factors, and a contribution of NOS in maintenance of urogenital structures has not previously been examined. Morphological changes in the corpora cavernosa occur at the same time as decreased NOS, suggesting a potential connection between decreased/inhibited NOS and morphological changes associated with ED. In this study we propose that NOS impacts urogenital morphology during development and will examine this hypothesis by NOS inhibition with L-NAME.

Methods: Primary outcomes were H&E, western and TUNEL to determine if penis, prostate and bladder morphology were altered with L-NAME treatment of Postnatal day 4 (P4) Sprague Dawley rats for 8 days. Tissue weight and immunohistochemical analysis for NOS were performed. Secondary evaluation of NOS-I regulation by Sonic Hedgehog (SHH) was examined by SHH inhibition in the Pelvic Ganglia (PG) and NOS-I protein was quantified by western in the PG/CN and penis. Nos abundance was quantified by RT-PCR during urogenital development and after CN injury.

Results: Apoptosis increased and penis, prostate and bladder morphology were altered with L-NAME. NOS inhibition decreased bladder weight 25%. SHH inhibition decreased NOS-I 35% in the PG/CN and 47% in the penis. Nos-III expression spiked within the first two weeks after birth in the penis but remained abundant in the adult. In the prostate, Nos-III was abundant immediately after birth and declined steadily with age. Nos-I expression in the PG/ CN decreased sharply with CN injury and returned to baseline by 7 days.

Conclusions: NOS is required for normal urogenital development. Since NOS is decreased with ED, it may contribute to the abnormal morphology observed in ED patients and animal models.

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