Effects of an alpha1A/D‐adrenoceptor antagonist, naftopidil, and a phosphodiesterase type 5 inhibitor, tadalafil, on urinary bladder remodeling in rats with spinal cord injury
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- Katsumi Kadekawa
- Department of Urology University of Pittsburgh School of Medicine Pittsburgh Pennsylvania
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- Tsuyoshi Majima
- Department of Urology University of Pittsburgh School of Medicine Pittsburgh Pennsylvania
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- Naoki Kawamorita
- Department of Urology University of Pittsburgh School of Medicine Pittsburgh Pennsylvania
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- Hiroki Okada
- Department of Urology University of Pittsburgh School of Medicine Pittsburgh Pennsylvania
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- Tsuyoshi Yoshizawa
- Department of Urology University of Pittsburgh School of Medicine Pittsburgh Pennsylvania
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- Kenichi Mori
- Department of Urology University of Pittsburgh School of Medicine Pittsburgh Pennsylvania
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- Pradeep Tyagi
- Department of Urology University of Pittsburgh School of Medicine Pittsburgh Pennsylvania
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- Kimio Sugaya
- Southern Knights’ Laboratory LLP Okinawa Japan
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- Naoki Yoshimura
- Department of Urology University of Pittsburgh School of Medicine Pittsburgh Pennsylvania
抄録
<jats:sec><jats:title>Aims</jats:title><jats:p>In order to clarify whether an alpha1A/D‐adrenoceptor (α<jats:sub>1</jats:sub>A/D‐AR) antagonist, naftopidil, or a phosphodiesterase type 5 (PDE5) inhibitor, tadalafil, prevents bladder wall remodeling after spinal cord injury (SCI), we examined the bladder and urethral activity as well as ischemic and fibrotic changes in the bladder using SCI rats with or without naftopidil or tadalafil treatment.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Adult female Sprague‐Dawley rats were divided into four groups: (1) normal (spinal cord intact); (2) vehicle SCI; (3) naftopidil SCI; and (4) tadalafil SCI groups. In SCI groups, rats underwent Th9‐10 spinal cord transection followed by oral application of vehicle, naftopidil (20 mg/kg/day) or tadalafil (2 mg/kg/day) for 1, 2, 4, 8, and 12 weeks. Bladder and urethral pressures, mRNA levels of fibrosis‐related molecules and ischemia markers and the composition of bladder collagen and elastin were evaluated.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>Naftopidil treatment reduced the upregulation of mRNA levels of ischemia and fibrosis markers at the early phase of SCI, and ameliorated the decrease of bladder compliance and voiding efficiency, and the increase of urethral pressure and collagen concentration in the bladder wall at the late phase of SCI. Tadalafil treatment reduced the upregulation of mRNA levels of fibrosis markers, the decrease of bladder compliance and the increase of collagen concentration at the late phase of SCI.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>These results suggest that naftopidil and tadalafil treatments improved the bladder remodeling shown by increased bladder collagen contents after SCI in a different time course. Thus, these treatments could be effective for reducing the SCI‐related tissue remodeling in the bladder. <jats:italic>Neurourol. Urodynam. 9999:XX–XX, 2016</jats:italic>. © 2016 Wiley Periodicals, Inc.</jats:p></jats:sec>
収録刊行物
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- Neurourology and Urodynamics
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Neurourology and Urodynamics 36 (6), 1488-1495, 2016-10-04
Wiley
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キーワード
詳細情報 詳細情報について
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- CRID
- 1362544418760863488
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- ISSN
- 15206777
- 07332467
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- データソース種別
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- Crossref