Hidenori Akaihata1, Masanori Nomiya2, Junya Hata2, Michihiro Yabe2, Norio Takahashi2, Nobuhiro Haga2, Nobuhiro Kushida2, Kei Ishibashi2, Ken Aikawa2, Osamu Yamaguchi2, Yoshiyuki Kojima2. 1. Department of Urology, Fukushima Medical University School of Medicine, Fukushima and Division of Bioengineering and LUTD Research, Nihon University School of Engineering (MN, OY), Koriyama, Japan. Electronic address: hidenoriakaihata@yahoo.co.jp. 2. Department of Urology, Fukushima Medical University School of Medicine, Fukushima and Division of Bioengineering and LUTD Research, Nihon University School of Engineering (MN, OY), Koriyama, Japan.
Abstract
PURPOSE: We investigated the effect of pelvic arterial occlusive disease on the RhoA/Rho-kinase pathway in a rat model of chronic bladder ischemia. MATERIALS AND METHODS: Male adult Sprague Dawley® rats at age 16 weeks were divided into arterial endothelial injury and control groups. The injury group underwent balloon endothelial injury of the bilateral iliac arteries and received a 2% cholesterol diet to induce pelvic arterial occlusive disease. The control group received a regular diet. At 8 weeks cystometrograms were performed. Bladder tissue was harvested for pharmacological studies and Western blot. RESULTS: Cystometrograms showed significantly lower bladder capacity in the arterial endothelial injury group than in controls. Organ bath studies revealed significantly decreased phasic contractions induced by carbachol in bladder strips from the injury group than from controls. In controls bladder strip tonic contractions induced by carbachol were significantly decreased compared with phasic contractions. However, no significant difference was observed between phasic and tonic contractions in the injury group. The Rho-kinase inhibitor Y-27632 produced a concentration dependent decrease in tonic contractions, which was more pronounced in the injury group. Western blot showed significantly increased RhoA and Rho-kinase β expression in the injury group. CONCLUSIONS: Our results suggest that pelvic arterial occlusive disease can affect the RhoA/Rho-kinase pathway in the bladder. This pathway might possibly be involved in the maintenance of tonic contraction and contribute to the bladder hyperactivity caused by pelvic arterial occlusive disease.
PURPOSE: We investigated the effect of pelvic arterial occlusive disease on the RhoA/Rho-kinase pathway in a rat model of chronic bladder ischemia. MATERIALS AND METHODS: Male adult Sprague Dawley® rats at age 16 weeks were divided into arterial endothelial injury and control groups. The injury group underwent balloon endothelial injury of the bilateral iliac arteries and received a 2% cholesterol diet to induce pelvic arterial occlusive disease. The control group received a regular diet. At 8 weeks cystometrograms were performed. Bladder tissue was harvested for pharmacological studies and Western blot. RESULTS: Cystometrograms showed significantly lower bladder capacity in the arterial endothelial injury group than in controls. Organ bath studies revealed significantly decreased phasic contractions induced by carbachol in bladder strips from the injury group than from controls. In controls bladder strip tonic contractions induced by carbachol were significantly decreased compared with phasic contractions. However, no significant difference was observed between phasic and tonic contractions in the injury group. The Rho-kinase inhibitor Y-27632 produced a concentration dependent decrease in tonic contractions, which was more pronounced in the injury group. Western blot showed significantly increased RhoA and Rho-kinase β expression in the injury group. CONCLUSIONS: Our results suggest that pelvic arterial occlusive disease can affect the RhoA/Rho-kinase pathway in the bladder. This pathway might possibly be involved in the maintenance of tonic contraction and contribute to the bladder hyperactivity caused by pelvic arterial occlusive disease.
Authors: Jae Heon Kim; Ji Sung Shim; Jong Wook Kim; Seung Whan Doo; Jae Hyun Bae; Ju Han Lee; Yun Seob Song; Je Jong Kim; Du Geon Moon Journal: World J Mens Health Date: 2019-06-14 Impact factor: 5.400