scholarly journals Detrusor Smooth Muscle KV7 Channels: Emerging New Regulators of Urinary Bladder Function

2020 ◽  
Vol 11 ◽  
Author(s):  
John Malysz ◽  
Georgi V. Petkov
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Bladder Function ◽  
Detrusor Smooth Muscle ◽  
Kv7 Channels

scholarly journals Urinary Bladder Contraction and Relaxation: Physiology and Pathophysiology

2004 ◽  
Vol 84 (3) ◽  
pp. 935-986 ◽  
Author(s):  
Karl-Erik Andersson ◽  
Anders Arner
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Bladder Wall ◽  
Outlet Obstruction ◽  
Hormonal Control ◽  
Membrane Properties ◽  
Bladder Function ◽  
Future Research ◽  
Detrusor Smooth Muscle ◽  
Functional Changes

The detrusor smooth muscle is the main muscle component of the urinary bladder wall. Its ability to contract over a large length interval and to relax determines the bladder function during filling and micturition. These processes are regulated by several external nervous and hormonal control systems, and the detrusor contains multiple receptors and signaling pathways. Functional changes of the detrusor can be found in several clinically important conditions, e.g., lower urinary tract symptoms (LUTS) and bladder outlet obstruction. The aim of this review is to summarize and synthesize basic information and recent advances in the understanding of the properties of the detrusor smooth muscle, its contractile system, cellular signaling, membrane properties, and cellular receptors. Alterations in these systems in pathological conditions of the bladder wall are described, and some areas for future research are suggested.

scholarly journals Oxidative Stress Contributes to Overactive Bladder in the Transgenic Sickle Cell Mouse

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 4582-4582
Author(s):  
Fabio Henrique Silva ◽  
Celso Saragosa Ramos Filho ◽  
Fabiano Beraldi Calmasini ◽  
Eduardo Costa Alexandre ◽  
Roger Barbosa Ferreira ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Overactive Bladder ◽  
Sickle Cell ◽  
Muscle Contractions ◽  
Bladder Function ◽  
Detrusor Smooth Muscle ◽  
Underactive Bladder ◽  
Response Curves ◽  
Smooth Muscle Contractions

Abstract Introduction: Lower urinary tract symptoms (LUTS) such as nocturia, urinary frequency, and urgency have been clinically reported in children and adults with sickle cell disease (SCD; Portocarrero et al J Urol 2012; Anele et al Neurourol Urodyn 2015), but little is known about the pathophysiology of micturition dysfunction in SCD patients. Transgenic sickle cell mice have been employed to better understand SCD pathophysiology. Recently, we reported that Berkeley SCD mice display underactive bladder and reduced detrusor smooth muscle contractions (Claudino et al Plos One, 2015). The homozygous Townes transgenic sickle cell mouse is another model for SCD, but urinary bladder dysfunction has never been studied in this model. Considering that SCD is associated with elevated ROS production, we hypothesized that increased ROS levels lead to alterations in the urinary bladder function of Townes SCD mice. Thus, the aim of this study was to evaluate the micturition and detrusor smooth muscle contractions in Townes transgenic sickle cell mice. Methods: Townes transgenic sickle cell mice and C57BL/6 mice (control) aged 3 to 4 months old were used. Cystometry was performed to evaluate the urinary function in vivo. In separate protocols, the urinary bladder was removed and placed in Krebs solution. Two longitudinal detrusor smooth muscle strips with intact urothelium were obtained from each bladder. The strips were mounted in 4-ml organ baths containing Krebs-Henseleit solution at 37°C continuously bubbled with a mixture of 95% O2 and 5% CO2 (pH 7.4). Cumulative concentration-response curves to muscarinic receptor agonist carbachol (CCh; 0.01-100 μM), chloride potassium (KCl; 1-300mM) and frequency-response curves for electrical field stimulation (EFS; 1-32Hz) were obtained in strips of detrusor smooth muscle from both control and SCD mice.mRNA expression for gp91phox and SOD-1 in bladder were also evaluated. Results: Micturition in SCD mice was irregular, and characterized by significant (P < 0.05) increases in the frequency of voiding contractions and nonvoiding contractions (n=5). Voiding pressure, basal pressure, capacity and threshold pressure were not changed in SCD mice. Carbachol (0.01 - 100 µM) induced concentration-dependent detrusor smooth muscle contractions in both control and SCD mice, but maximal contractile responses were significantly lower (P < 0.05) in SCD compared to control mice (1.40 ± 0.4 and 2.9 ± 0.2 mN/mg, respectively; n=5). Likewise, EFS-induced neurogenic detrusor contractions in SCD mice were 29% lower (P < 0.05) compared to the control (n=10). Contractile responses induced by KCl (1 - 300 mM) did not differ between control and SCD group (n=5). The mRNA expression for the NADPH subunit gp91phox in bladder was about 2-fold higher (P<0.05) in SCD mice compared to the control group, whereas no changes in the mRNA expression for SOD-1 were observed among groups (n=6). Infiltration by inflammatory cells (mononuclear cells) was seen in the submucosa and muscular area of bladder from SCD mice (n=4). Conclusion: Our study shows that the overactive bladder seen in SCD mouse is associated with upregulation of NADPH oxidase subunit gp91phox. Interestingly, in the contrast, the Berkeley SCD mouse exhibits an atonic detrusor smooth muscle and underactive bladder (Claudino et al Plos One 2015). One may speculate therefore that the overactive bladder in Townes SCD may progress to underactive bladder at latter stages. To confirm this hypothesis, we will evaluate the urinary bladder function in older SCD mice. Financial Support: FAPESP Disclosures No relevant conflicts of interest to declare.

Phosphorylation of extracellular signal-regulated kinases in urinary bladder in rats with cyclophosphamide-induced cystitis

2007 ◽  
Vol 293 (1) ◽  
pp. R125-R134 ◽  
Author(s):  
Kimberly A. Corrow ◽  
Margaret A. Vizzard
Keyword(s):  
Urinary Bladder ◽  
Chronic Treatment ◽  
Bladder Capacity ◽  
Nerve Fibers ◽  
Bladder Function ◽  
Detrusor Smooth Muscle ◽  
Erk Phosphorylation ◽  
Extracellular Signal ◽  
Perk Expression ◽  
Whole Mount

Phosphorylated ERK expression has been demonstrated in the central and peripheral nervous system after various stimuli, including visceral stimulation. Changes in the activation (i.e., phosphorylation) of extracellular signal-regulated kinases (pERK) were examined in the urinary bladder after 4 h (acute), 48 h (intermediate), or chronic (10 day) cyclophosphamide (CYP) treatment. CYP-induced cystitis significantly ( P ≤ 0.01) increased pERK expression in the urinary bladder with intermediate (48 h) and chronic CYP treatment. Immunohistochemistry for pERK immunoreactivity revealed little pERK-IR in control or acute (4 h) CYP-treated rat urinary bladders. However, pERK expression was significantly ( P ≤ 0.01) upregulated in the urothelium after 48 h or chronic CYP treatment. Whole mount preparations of urothelium/lamina propria or detrusor smooth muscle from control (noninflamed) rats showed no pERK-IR in PGP9.5-labeled nerve fibers in the suburothelial plexus. However, with CYP-treatment (48 h, chronic), a few pERK-IR nerve fibers in the suburothelial plexus of whole mount preparations of bladder and at the serosal edge of urinary bladder sections were observed. pERK-IR cells expressing the CD86 antigen were also observed in urinary bladder from CYP-treated rats (48 h, chronic). Treatment with the upstream inhibitor of ERK phosphorylation, U0126, significantly ( P ≤ 0.01) increased bladder capacity in CYP-treated rats (48 h). These studies suggest that therapies targeted at pERK pathways may improve urinary bladder function in CYP-treated rats.

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