New concepts in relation to urge and detrusor activity

Coolsaet, B.L.R.A.; Duyl, W. A. van; Os-Bossagh, P. van; Bakker, Hans V. De

doi:10.1002/nau.1930120504

Cited by 124 publications

(126 citation statements)

References 23 publications

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“…The high occurrence of NVCs could be a compensatory mechanism to increase afferent firing in an attempt to initiate voiding. Other authors have already proposed a similar idea of active contribution of NVCs to afferent signaling (35,36).…”

Section: Discussionmentioning

confidence: 92%

Deletion of the transient receptor potential cation channel TRPV4 impairs murine bladder voiding

Gevaert¹,

Vriens²,

Segal³

et al. 2007

J. Clin. Invest.

295

349

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Here we provide evidence for a critical role of the transient receptor potential cation channel, subfamily V, member 4 (TRPV4) in normal bladder function. Immunofluorescence demonstrated TRPV4 expression in mouse and rat urothelium and vascular endothelium, but not in other cell types of the bladder. Intracellular Ca 2+ measurements on urothelial cells isolated from mice revealed a TRPV4-dependent response to the selective TRPV4 agonist 4α-phorbol 12,13-didecanoate and to hypotonic cell swelling. Behavioral studies demonstrated that TRPV4 -/-mice manifest an incontinent phenotype but show normal exploratory activity and anxietyrelated behavior. Cystometric experiments revealed that TRPV4 -/-mice exhibit a lower frequency of voiding contractions as well as a higher frequency of nonvoiding contractions. Additionally, the amplitude of the spontaneous contractions in explanted bladder strips from TRPV4 -/-mice was significantly reduced. Finally, a decreased intravesical stretch-evoked ATP release was found in isolated whole bladders from TRPV4 -/-mice. These data demonstrate a previously unrecognized role for TRPV4 in voiding behavior, raising the possibility that TRPV4 plays a critical role in urothelium-mediated transduction of intravesical mechanical pressure.

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Section: Discussionmentioning

confidence: 92%

Deletion of the transient receptor potential cation channel TRPV4 impairs murine bladder voiding

Gevaert¹,

Vriens²,

Segal³

et al. 2007

J. Clin. Invest.

295

349

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show abstract

“…These small, spontaneous nonvoiding contractions, which occur in parts of the bladder wall, have also been called micromotions (11) or microtransients (16). These events may be important during the filling phase, playing a role in adjusting the length of smooth muscle fibers in response to filling (7) or communicating information on bladder fullness (11,16,22). Because the contractile force of muscularis mucosae contractions is ϳ40 times less than that of the detrusor, these events would be expected to contribute minimally to micturition.…”

Section: R359mentioning

confidence: 99%

Unique properties of muscularis mucosae smooth muscle in guinea pig urinary bladder

Heppner¹,

Layne²,

Pearson³

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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The muscularis mucosae, a type of smooth muscle located between the urothelium and the urinary bladder detrusor, has been described, although its properties and role in bladder function have not been characterized. Here, using mucosal tissue strips isolated from guinea pig urinary bladders, we identified spontaneous phasic contractions (SPCs) that appear to originate in the muscularis mucosae. This smooth muscle layer exhibited Ca 2ϩ waves and flashes, but localized Ca 2ϩ events (Ca 2ϩ sparks, purinergic receptor-mediated transients) were not detected. Ca 2ϩ flashes, often in bursts, occurred with a frequency (ϳ5.7/min) similar to that of SPCs (ϳ4/min), suggesting that SPCs are triggered by bursts of Ca 2ϩ flashes. The force generated by a single mucosal SPC represented the maximal force of the strip, whereas a single detrusor SPC was ϳ3% of maximal force of the detrusor strip. Electrical field stimulation (0.5-50 Hz) evoked force transients in isolated detrusor and mucosal strips. Inhibition of cholinergic receptors significantly decreased force in detrusor and mucosal strips (at higher frequencies). Concurrent inhibition of purinergic and cholinergic receptors nearly abolished evoked responses in detrusor and mucosae. Mucosal SPCs were unaffected by blocking smallconductance Ca 2ϩ -activated K ϩ (SK) channels with apamin and were unchanged by blocking large-conductance Ca 2ϩ -activated K ϩ (BK) channels with iberiotoxin (IbTX), indicating that SK and BK channels play a much smaller role in regulating muscularis mucosae SPCs than they do in regulating detrusor SPCs. Consistent with this, BK channel current density in myocytes from muscularis mucosae was ϳ20% of that in detrusor myocytes. These findings indicate that the muscularis mucosae in guinea pig represents a second smooth muscle compartment that is physiologically and pharmacologically distinct from the detrusor and may contribute to the overall contractile properties of the urinary bladder. calcium imaging; large-conductance calcium-activated potassium channel; potassium channels; calcium flashes; spontaneous phasic contractions THE URINARY BLADDER is a hollow, muscular organ that serves two functions: urine storage and elimination. The bladder wall is composed of detrusor smooth muscle, which accounts for a large fraction of the bladder mass, and a layer of transitional epithelial cells known as the urothelium, which lines the luminal surface of the urinary bladder. The detrusor smooth muscle has been extensively characterized and is clearly responsible for the majority of the contractile properties of the urinary bladder (1, 69). The urothelium, which was originally thought to simply act as a passive, impermeable barrier that prevents the movement of solutes from the urine into the bloodstream, is now recognized to possess a broad range of sensory and signal transduction functions that greatly influence bladder physiology (for a review, see Ref. 5).The detrusor exhibits two primary modes of contractile behavior: nerve-evoked contractions and spontaneo...

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“…In bladder irritation caused by structural obstructhat the underlying reason for this phenomenon is not an isovolumetry but rather a deficiency in nervous tion or in neurogenic hyper-reflexia or areflexia, there is no sensory or motor diCerence either (Hohlbrugger, recruitment for the synchronicity of the individual detrusor muscle contractions, comparable with ventricuunpublished results). If a pressure-flow study is performed after cystometry, dysfunctional voiding caused lar fibrillation [9]. Hence, the diagnostic diCerentiation between hypersensitivity and hyperactivity (instability) by K+ is diagnosed three times more often than with conventional NaCl-filling [10].…”

Section: Gradients In the Bladdermentioning

confidence: 99%

Urinary potassium and the overactive bladder

Hohlbrugger

1999

BJU International

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New concepts in relation to urge and detrusor activity

Cited by 124 publications

References 23 publications

Deletion of the transient receptor potential cation channel TRPV4 impairs murine bladder voiding

Deletion of the transient receptor potential cation channel TRPV4 impairs murine bladder voiding

Unique properties of muscularis mucosae smooth muscle in guinea pig urinary bladder

Urinary potassium and the overactive bladder

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