scholarly journals Role of desmin in active force transmission and maintenance of structure during growth of urinary bladder

2008 ◽  
Vol 295 (2) ◽  
pp. C324-C331 ◽  
Author(s):  
R. Sjuve Scott ◽  
Z. Li ◽  
D. Paulin ◽  
B. Uvelius ◽  
J. V. Small ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Structural Changes ◽  
Wall Structure ◽  
Intermediate Filament Protein ◽  
Active Force ◽  
Force Transmission ◽  
Bladder Smooth Muscle ◽  
Shortening Velocity

Role of the intermediate filament protein desmin in hypertrophy of smooth muscle was examined in desmin-deficient mice (Des−/−). A partial obstruction of the urethra was created, and after 9–19 days bladder weight increased approximately threefold in both Des−/− and wild type (Des+/+) animals. Bladder growth was associated with the synthesis of actin and myosin. In the hypertrophic Des+/+ bladder, the relative content of desmin increased. In Des−/−mice, desmin was absent. No alterations in the amount of vimentin were observed. Although Des−/− obstructed bladders were capable of growth, they had structural changes with a partial disruption of the wall. Des−/−bladders had slightly lower passive stress and significantly lower active stress compared with Des+/+. Des−/−preparations had lower shortening velocity. During hypertrophy, these structural and mechanical alterations in the Des−/−urinary bladder became more pronounced. In conclusion, desmin in the bladder smooth muscle is not needed for growth but has a role in active force transmission and maintenance of wall structure.

scholarly journals Expression and functional role of Rho-kinase in rat urinary bladder smooth muscle

2003 ◽  
Vol 138 (5) ◽  
pp. 757-766 ◽  
Author(s):  
Alexandra Wibberley ◽  
Zunxuan Chen ◽  
Erding Hu ◽  
J Paul Hieble ◽  
Timothy D Westfall
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Functional Role ◽  
Rho Kinase ◽  
Bladder Smooth Muscle ◽  
Rat Urinary Bladder ◽  
Urinary Bladder Smooth Muscle

scholarly journals Stimulation of β3-adrenoceptors relaxes rat urinary bladder smooth muscle via activation of the large-conductance Ca2+-activated K+ channels

2008 ◽  
Vol 295 (5) ◽  
pp. C1344-C1353 ◽  
Author(s):  
Kiril L. Hristov ◽  
Xiangli Cui ◽  
Sean M. Brown ◽  
Lei Liu ◽  
Whitney F. Kellett ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Bk Channels ◽  
Bk Channel ◽  
Bladder Smooth Muscle ◽  
Rat Urinary Bladder ◽  
Urinary Bladder Smooth Muscle ◽  
Brl 37344 ◽  
Stimulation Of

We investigated the role of large-conductance Ca2+-activated K+ (BK) channels in β3-adrenoceptor (β3-AR)-induced relaxation in rat urinary bladder smooth muscle (UBSM). BRL 37344, a specific β3-AR agonist, inhibits spontaneous contractions of isolated UBSM strips. SR59230A, a specific β3-AR antagonist, and H89, a PKA inhibitor, reduced the inhibitory effect of BRL 37344. Iberiotoxin, a specific BK channel inhibitor, shifts the BRL 37344 concentration response curves for contraction amplitude, net muscle force, and tone to the right. Freshly dispersed UBSM cells and the perforated mode of the patch-clamp technique were used to determine further the role of β3-AR stimulation by BRL 37344 on BK channel activity. BRL 37344 increased spontaneous, transient, outward BK current (STOC) frequency by 46.0 ± 20.1%. In whole cell mode at a holding potential of Vh = 0 mV, the single BK channel amplitude was 5.17 ± 0.28 pA, whereas in the presence of BRL 37344, it was 5.55 ± 0.41 pA. The BK channel open probability was also unchanged. In the presence of ryanodine and nifedipine, the current-voltage relationship in response to depolarization steps in the presence and absence of BRL 37344 was identical. In current-clamp mode, BRL 37344 caused membrane potential hyperpolarization from −26.1 ± 2.1 mV (control) to −29.0 ± 2.2 mV. The BRL 37344-induced hyperpolarization was eliminated by application of iberiotoxin, tetraethylammonium or ryanodine. The data indicate that stimulation of β3-AR relaxes rat UBSM by increasing the BK channel STOC frequency, which causes membrane hyperpolarization and thus relaxation.

scholarly journals Constitutive PKA activity is essential for maintaining the excitability and contractility in guinea pig urinary bladder smooth muscle: role of the BK channel

2014 ◽  
Vol 307 (12) ◽  
pp. C1142-C1150 ◽  
Author(s):  
Wenkuan Xin ◽  
Ning Li ◽  
Qiuping Cheng ◽  
Vitor S. Fernandes ◽  
Georgi V. Petkov
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Fluorescence Microscopy ◽  
Guinea Pig ◽  
Bk Channels ◽  
Bk Channel ◽  
Bladder Smooth Muscle ◽  
Ratiometric Fluorescence ◽  
Urinary Bladder Smooth Muscle

The elevation of protein kinase A (PKA) activity activates the large-conductance voltage- and Ca2+-activated K+ (BK) channels in urinary bladder smooth muscle (UBSM) cells and consequently attenuates spontaneous phasic contractions of UBSM. However, the role of constitutive PKA activity in UBSM function has not been studied. Here, we tested the hypothesis that constitutive PKA activity is essential for controlling the excitability and contractility of UBSM. We used patch clamp electrophysiology, line-scanning confocal and ratiometric fluorescence microscopy on freshly isolated guinea pig UBSM cells, and isometric tension recordings on freshly isolated UBSM strips. Pharmacological inhibition of the constitutive PKA activity with H-89 or PKI 14–22 significantly reduced the frequency and amplitude of spontaneous transient BK channel currents (TBKCs) in UBSM cells. Confocal and ratiometric fluorescence microscopy studies revealed that inhibition of constitutive PKA activity with H-89 reduced the frequency and amplitude of the localized Ca2+ sparks but increased global Ca2+ levels and the magnitude of Ca2+ oscillations in UBSM cells. H-89 abolished the spontaneous transient membrane hyperpolarizations and depolarized the membrane potential in UBSM cells. Inhibition of PKA with H-89 or KT-5720 also increased the amplitude and muscle force of UBSM spontaneous phasic contractions. This study reveals the novel concept that constitutive PKA activity is essential for controlling localized Ca2+ signals generated by intracellular Ca2+ stores and cytosolic Ca2+ levels. Furthermore, constitutive PKA activity is critical for mediating the spontaneous TBKCs in UBSM cells, where it plays a key role in regulating spontaneous phasic contractions in UBSM.

Low levels of KATP channel activation decrease excitability and contractility of urinary bladder

2001 ◽  
Vol 280 (5) ◽  
pp. R1427-R1433 ◽  
Author(s):  
Georgi V. Petkov ◽  
Thomas J. Heppner ◽  
Adrian D. Bonev ◽  
Gerald M. Herrera ◽  
Mark T. Nelson
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Action Potentials ◽  
Critical Issue ◽  
Bladder Smooth Muscle ◽  
Channel Activation ◽  
Smooth Muscle Function ◽  
Urinary Bladder Smooth Muscle ◽  
Channel Currents

Activation of ATP-sensitive potassium (KATP) channels can regulate smooth muscle function through membrane potential hyperpolarization. A critical issue in understanding the role of KATP channels is the relationship between channel activation and the effect on tissue function. Here, we explored this relationship in urinary bladder smooth muscle (UBSM) from the detrusor by activating KATP channels with the synthetic compounds N-(4-benzoylphenyl)-3,3,3-trifluoro-2-hydroxy-2-methylpropionamide (ZD-6169) and levcromakalim. The effects of ZD-6169 and levcromakalim on KATP channel currents in isolated UBSM cells, on action potentials, and on related phasic contractions of isolated UBSM strips were examined. ZD-6169 and levcromakalim at 1.02 and 2.63 μM, respectively, caused half-maximal activation (K1/2) of KATP currents in single UBSM cells (see Heppner TJ, Bonev A, Li JH, Kau ST, and Nelson MT. Pharmacology 53: 170–179, 1996). In contrast, much lower concentrations (K1/2 = 47 nM for ZD-6169 and K1/2 = 38 nM for levcromakalim) caused inhibition of action potentials and phasic contractions of UBSM. The results suggest that activation of <1% of KATP channels is sufficient to inhibit significantly action potentials and the related phasic contractions.

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