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

The effect of chronic partial bladder outlet obstruction on corpus cavernosum smooth muscle and Rho-kinase in rabbits

2008 ◽  
Vol 27 (8) ◽  
pp. 826-831 ◽  
Author(s):  
Wei-Yu Lin ◽  
Anita Mannikarottu ◽  
Paul Chichester ◽  
Paul Neuman ◽  
Arnold Johnson ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Bladder Outlet Obstruction ◽  
Corpus Cavernosum ◽  
Rho Kinase ◽  
Outlet Obstruction ◽  
Partial Bladder Outlet Obstruction

scholarly journals Adjustable passive stiffness in mouse bladder: regulated by Rho kinase and elevated following partial bladder outlet obstruction

2012 ◽  
Vol 302 (8) ◽  
pp. F967-F976 ◽  
Author(s):  
John E. Speich ◽  
Jordan B. Southern ◽  
Sheree Henderson ◽  
Cameron W. Wilson ◽  
Adam P. Klausner ◽  
...  
Keyword(s):  
Bladder Outlet Obstruction ◽  
Bladder Wall ◽  
Rho Kinase ◽  
Outlet Obstruction ◽  
Prostaglandin E ◽  
Passive Stiffness ◽  
Regulatory Pathways ◽  
Partial Bladder Outlet Obstruction ◽  
Length Changes ◽  
Adjustable Passive Stiffness

Detrusor smooth muscle (DSM) contributes to bladder wall tension during filling, and bladder wall deformation affects the signaling system that leads to urgency. The length-passive tension ( L-Tp) relationship in rabbit DSM can adapt with length changes over time and exhibits adjustable passive stiffness (APS) characterized by a L-Tpcurve that is a function of both activation and strain history. Muscle activation with KCl, carbachol (CCh), or prostaglandin E2at short muscle lengths can increase APS that is revealed by elevated pseudo-steady-state Tpat longer lengths compared with prior Tpmeasurements at those lengths, and APS generation is inhibited by the Rho Kinase (ROCK) inhibitor H-1152. In the current study, mouse bladder strips exhibited both KCl- and CCh-induced APS. Whole mouse bladders demonstrated APS which was measured as an increase in pressure during passive filling in calcium-free solution following CCh precontraction compared with pressure during filling without precontraction. In addition, CCh-induced APS in whole mouse bladder was inhibited by H-1152, indicating that ROCK activity may regulate bladder compliance during filling. Furthermore, APS in whole mouse bladder was elevated 2 wk after partial bladder outlet obstruction, suggesting that APS may be relevant in diseases affecting bladder mechanics. The presence of APS in mouse bladder will permit future studies of APS regulatory pathways and potential alterations of APS in disease models using knockout transgenetic mice.

scholarly journals Effect of Age on the Role of Rho-Kinase in Short-term Partial Bladder Outlet Obstruction

Urology ◽  
2008 ◽  
Vol 71 (3) ◽  
pp. 541-545 ◽  
Author(s):  
Ahmet Guven ◽  
Wei-Yu Lin ◽  
Paul Neuman ◽  
Barry A. Kogan ◽  
Robert Levin ◽  
...  
Keyword(s):  
Bladder Outlet Obstruction ◽  
Rho Kinase ◽  
Outlet Obstruction ◽  
Short Term ◽  
Partial Bladder Outlet Obstruction ◽  
Effect Of Age

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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