Changes of Detrusor Contractility after Partial Bladder Outlet Obstruction and Relief of Obstruction in Rat: Long-term Evaluation

2000 ◽  
Vol 4 (1) ◽  
pp. 30
Author(s):  
Joon Chul Kim ◽  
Jai Young Yoon ◽  
Tae Kon Hwang ◽  
Dong Hwan Lee ◽  
Seong Il Seo ◽  
...  
Keyword(s):  
Bladder Outlet Obstruction ◽  
Outlet Obstruction ◽  
Partial Bladder Outlet Obstruction ◽  
Detrusor Contractility ◽  
Term Evaluation

Long term partial bladder outlet obstruction induced contractile dysfunction in male rabbits: A role for Rho-kinase

2007 ◽  
Vol 26 (7) ◽  
pp. 1043-1049 ◽  
Author(s):  
Ahmet Guven ◽  
Bulent Onal ◽  
Carmin Kalorin ◽  
Catherine Whitbeck ◽  
Paul Chichester ◽  
...  
Keyword(s):  
Bladder Outlet Obstruction ◽  
Rho Kinase ◽  
Outlet Obstruction ◽  
Contractile Dysfunction ◽  
Partial Bladder Outlet Obstruction

scholarly journals AMPK Alters Detrusor Contractility During Emptying in Normal Bladder and Hypertrophied Bladder with Partial Bladder Outlet Obstruction via CaMKKβ

2019 ◽  
Vol 20 (11) ◽  
pp. 2650
Author(s):  
Bo-Hwa Choi ◽  
Long-Hu Jin ◽  
Doo Yong Chung ◽  
Tae Jin Cho ◽  
Ju-Hee Kang ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Bladder Outlet Obstruction ◽  
Contractile Response ◽  
Outlet Obstruction ◽  
Ampk Signaling ◽  
Partial Bladder Outlet Obstruction ◽  
Compound C ◽  
Detrusor Contractility ◽  
Normal Bladder

AMP-activated protein kinase (AMPK) has been implicated in contractility changes in bladders with partial bladder outlet obstruction (PBOO), but the role of AMPK in the contractile response of normal bladder remains unclear. We investigated the phosphorylation of AMPKα and expression of the involved upstream AMPK kinases (AMPKKs) in a model of bladders with PBOO and sought to determine whether the pharmacological inhibition of these two factors affected detrusor contractility in normal bladders, using female Sprague–Dawley rats. Cystometry and Western blot analysis were performed in rats that were subjected to PBOO induction or a sham operation. Cystometry was performed in normal rats that received selective inhibitors of AMPKα and Ca2+/calmodulin-dependent protein kinase kinase (CaMKKβ) (compound C and STO-609, respectively) at doses determined in the experiments. In the PBOO bladders, bladder weight and micturition pressure (MP) were higher and AMPKα phosphorylation (T172) and CaMKKβ expression was significantly reduced. Compound C and STO-609 increased MP. The increased contractile response in bladders with PBOO-induced hypertrophy was related to decreased CaMKKβ/AMPK signaling activity, and the pharmacological inhibition of this pathway in normal bladders increased detrusor contractility, implying a role of CaMKKβ/AMPK signaling in the bladder in the regulation of detrusor contractility.

Metformin ameliorates bladder dysfunction in a rat model of partial bladder outlet obstruction

2021 ◽  
Vol 320 (5) ◽  
pp. F838-F858
Author(s):  
Lipeng Chen ◽  
Linchen Lv ◽  
Lekai Zhang ◽  
Zhengdong Gao ◽  
Yaxiao Liu ◽  
...  
Keyword(s):  
Clinical Trials ◽  
Rat Model ◽  
Bladder Outlet Obstruction ◽  
Bladder Dysfunction ◽  
Outlet Obstruction ◽  
Term Treatment ◽  
Potential Drug ◽  
Partial Bladder Outlet Obstruction ◽  
Long Term Treatment

The present study in a rat model showed that oral administration of metformin alleviated inflammation following partial bladder outlet obstruction in the early phase and ameliorated bladder fibrosis as well as bladder dysfunction by long-term treatment. Our study indicated that metformin is a potential drug to inhibit bladder remodeling and alleviate bladder dysfunction. Clinical trials are needed to validate the effect of metformin on the bladder dysfunction and bladder fibrosis in the future.

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