scholarly journals AB283. SPR-10 Down-regulation of ryanodine receptor gene expression in murine urinary bladder smooth muscle following partial bladder outlet obstruction

2016 ◽  
Vol 5 (S2) ◽  
pp. AB283-AB283
Author(s):  
Ettickan Boopathi ◽  
Elham Javed ◽  
Shankar Addya ◽  
Paolo Fortina ◽  
Stephen Zderic ◽  
...  
Keyword(s):  
Gene Expression ◽  
Smooth Muscle ◽  
Urinary Bladder ◽  
Bladder Outlet Obstruction ◽  
Receptor Gene ◽  
Outlet Obstruction ◽  
Bladder Smooth Muscle ◽  
Partial Bladder Outlet Obstruction ◽  
Urinary Bladder Smooth Muscle ◽  
Receptor Gene Expression

Partial bladder outlet obstruction alters Ca2+ sensitivity of force, but not of MLC phosphorylation, in bladder smooth muscle

2003 ◽  
Vol 285 (4) ◽  
pp. F703-F710 ◽  
Author(s):  
Michaela C. Stanton ◽  
Michele Clement ◽  
Edward J. Macarak ◽  
Stephen A. Zderic ◽  
Robert S. Moreland
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Bladder Outlet Obstruction ◽  
Outlet Obstruction ◽  
Muscle Cells ◽  
Maximal Velocity ◽  
Bladder Smooth Muscle ◽  
Partial Bladder Outlet Obstruction ◽  
Velocity Of Shortening ◽  
Mlc Phosphorylation

Partial bladder outlet obstruction in the rabbit produces changes in bladder function similar to those seen clinically in patients with obstructive uropathies. Whole organ function is significantly altered, as are the smooth muscle cells inside the bladder wall. This study was designed to determine whether outlet obstruction alters smooth muscle function at the level of contractile filaments. Rabbit bladders were partially obstructed for 2 wk. Triton X-100 was used to provide a detergent-skinned bladder smooth muscle preparation that would allow control of the intracellular environment while the ability to shorten and develop force is maintained. Ca2+-force and Ca2+-myosin light chain (MLC) phosphorylation relations and maximal velocity of shortening were determined. The Ca2+ sensitivity of force was significantly lower in tissues from animals subjected to outlet obstruction compared with tissues from control animals. In contrast, no difference was noted in the Ca2+ sensitivity of MLC phosphorylation. Maximal levels of stress and MLC phosphorylation were similar in both animal groups. Maximal velocity of shortening was significantly slower in tissues from outlet-obstructed animals at all Ca2+ concentrations compared with tissues from control animals. Ultrastructurally, detergent skinning had little effect on structural integrity. Moreover, tissues from obstructed animals showed an increase in the number of sarcolemmal attachment plaque structures. We suggest that partial bladder outlet obstruction produces deleterious (e.g., decrease in Ca2+ sensitivity of force) and compensatory (e.g., increase in membrane attachment plaques) changes in bladder smooth muscle cells.

The Fate of Urinary Bladder Smooth Muscle After Outlet Obstruction—A Role for the Sarcoplasmic Reticulum

2003 ◽  
pp. 773-790 ◽  
Author(s):  
Raimund Stein ◽  
ChaoLiang Gong ◽  
Joel Hutcheson ◽  
Lev Krasnopolsky ◽  
Douglas A. Canning ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Urinary Bladder ◽  
Outlet Obstruction ◽  
Bladder Smooth Muscle ◽  
Urinary Bladder Smooth Muscle

Partial bladder outlet obstruction abolishes the receptor- and G protein-dependent increase in calcium sensitivity in rabbit bladder smooth muscle

2004 ◽  
Vol 287 (4) ◽  
pp. F682-F689 ◽  
Author(s):  
Michaela C. Stanton ◽  
Daniel Delaney ◽  
Stephen A. Zderic ◽  
Robert S. Moreland
Keyword(s):  
Smooth Muscle ◽  
Animal Models ◽  
G Protein ◽  
Bladder Outlet Obstruction ◽  
Statistical Significance ◽  
Outlet Obstruction ◽  
Calcium Sensitivity ◽  
Bladder Smooth Muscle ◽  
Protein Activity ◽  
Partial Bladder Outlet Obstruction

Partial bladder outlet obstruction (PBOO) alters the function of the whole bladder and produces specific alterations in the contractility of the bladder smooth muscle cell. The goal of this study was to test the hypothesis that PBOO affects smooth muscle contraction at the level of the receptor- and G protein-dependent increase in myofilament Ca2+ sensitivity. To address this question, we used α-toxin-permeabilized strips of bladder smooth muscle from control animals and animals subjected to 2 wk of PBOO. Increasing free [Ca2+] increased force in permeabilized strips from control animals; the addition of 10 μM carbachol and 10 μM GTP increased both the Ca2+ sensitivity of the contractions and the maximal levels of force attained. In contrast, although increases in [Ca2+] increased force in permeabilized strips from PBOO animals, the addition of carbachol and GTP had no additional effects. Myosin light chain phosphorylation levels increased with [Ca2+], and although they tended to be higher in strips from PBOO animals, they did not reach statistical significance. Assessment of G protein activity from both animal models suggests this is not a site responsible for the loss of carbachol and GTP enhancement of myofilament Ca2+ sensitivity. The addition of phorbol dibutyrate increased the Ca2+ sensitivity of force development in strips from both animal models, suggesting that an alteration in PKC signaling is not involved. Our results are consistent with the hypothesis that PBOO decreases receptor-mediated myofilament calcium sensitization and that the site of action is downstream from either the G proteins or PKC.

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