Urinary Bladder Contraction and Relaxation: Physiology and Pathophysiology

Andersson, Karl‐Erik; Arner, Anders

doi:10.1152/physrev.00038.2003

Cited by 786 publications

(769 citation statements)

References 724 publications

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“…The stretch receptors in the bladder wall sense bladder fullness, and convey signals via the afferent fibers of the pelvic nerve toward the spinal cord and the brainstem 32, 33, 34. The periaqueductal gray and pontine micturition center regions in the brainstem integrate the afferent signals, and upon bladder fullness, initiate the micturition process by sending down descending inputs to the sacral spinal cord to contract the bladder detrusor muscles and relax the sphincter muscles.…”

Section: The Sma‐based Device For Myogenic Uabmentioning

confidence: 99%

“…Excitation of the autonomic efferent fibers of the pelvic nerve by the descending inputs leads to contraction of the detrusor muscle and relaxation of the internal urethral sphincter required for voiding. Inhibition of the somatic pudendal pathway by the descending inputs results in relaxation of the external urethra sphincter muscles 32, 33, 34…”

Section: The Sma‐based Device For Myogenic Uabmentioning

confidence: 99%

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A 3D Printed Implantable Device for Voiding the Bladder Using Shape Memory Alloy (SMA) Actuators

et al. 2017

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Underactive bladder or detrusor underactivity (DU) is defined as a reduction of contraction strength or duration of the bladder wall. Despite the serious healthcare implications of DU, there are limited solutions for affected individuals. A flexible 3D printed implantable device driven by shape memory alloys (SMA) actuators is presented here for the first time to physically contract the bladder to restore voluntary control of the bladder for individuals suffering from DU. This approach is used initially in benchtop experiments with a rubber balloon acting as a model for the rat bladder to verify its potential for voiding, and that the operating temperatures are safe for the eventual implantation of the device in a rat. The device is then implanted and tested on an anesthetized rat, and a voiding volume of more than 8% is successfully achieved for the SMA‐based device without any surgical intervention or drug injection to relax the external sphincter.

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Section: The Sma‐based Device For Myogenic Uabmentioning

confidence: 99%

Section: The Sma‐based Device For Myogenic Uabmentioning

confidence: 99%

A 3D Printed Implantable Device for Voiding the Bladder Using Shape Memory Alloy (SMA) Actuators

et al. 2017

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“…The resulting functional outlet obstruction causes bladder distension and detrusor hypertrophy 13 . These changes elicit profound, long-lasting alterations in the pattern of autonomic bladder innervation, which leads to a pathological increase in neural excitability 2,14 .…”

Section: Formation Of Neurogenic Bladder Dysfunctionmentioning

confidence: 99%

Multisystem Neuroprosthetic Training Improves Bladder Function After Severe Spinal Cord Injury

et al. 2013

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BACKGROUND: Severe spinal cord injury (SCI) leads to neurogenic bladder dysfunction. We recently developeda multi-system neuroprosthetic training program (MSNT) that promotes plastic changes capable of restoring refinedlocomotion in rats with severe SCI. We investigated whether MSNTinfluences the formation of posttraumatic bladder dysfunction. MATERIALS AND METHODS: Adult rats were randomly assigned to a SCI (n=8) and to a control intact (n=4) group. SCI consisted of two opposite lateral hemisections (T7, T11), thusinterrupting all direct supraspinal input. After SCI, 4 rats were subjected to MSNT, 4 rats were non-trained. After 8 weekswe performed urodynamics and evaluated kidney function (creatinine, cystatin C). Bladder investigation included morphological, histological and immunohistochemical evaluations. RESULTS: Bladder capacity increased 3-fold in trained and 7-fold in non-trained compared to intact animals. During filling,we found 2.7 ± 1.1 non-voiding contractions (NVC) in trained, compared to 12.6 ± 5.2 in non-trained rats. Bladder morphology was similar in trained and intact rats, non-trained ratsexhibited detrusor hypertrophycharacterized by increased detrusor thickness and decreased connective tissue to smooth muscle ratio. The general nerve density, labeled with PGP9.5, was significantly increased in trained and significantly decreased in non-trained rats. The relative proportion of NF200-postive afferent nerves was significantly lower in trained compared to intact and non-trained rats. NPY-positive fibers showed a significantly lower density in non-trained rats. CONCLUSIONS: MSNT effectively counteracts the formation of neurogenic bladder dysfunction after severe SCI and might contribute to preserving bladder function and preventing long-term complications in patients with severe SCI. MULTI-SYSTEM NEUROPROSTHETIC TRAINING IMPROVES BLADDER FUNCTION AFTER SEVERE SPINAL CORD INJURY

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“…72,73 In conditions of increased sensory nerve transmission after chronic inflammation and spinal cord injury, 74 increased release of ATP from the urothelium might activate the ATP receptor P2X 3 in epithelial and subepithelial layers to increase afferent nerve activity, which would account for the higher frequency of bladder contractions that are reported in both human and animal models of spinal cord injury. 74 A study in 2004 showed that BTX-A inhibits ATP release from the urothelial but not the serosal side of the bladder, suggesting that BTX-A inhibits transmitter release not only from efferent nerve endings but from sensory nerve terminals or urothelium as well.…”

Section: Effects On Acetylcholine and Atp Releasementioning

confidence: 99%

Drug Insight: biological effects of botulinum toxin A in the lower urinary tract

et al. 2008

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SUMMARYBotulinum toxins can effectively and selectively disrupt and modulate neurotransmission in striated muscle. Recently, urologists have become interested in the use of these toxins in patients with detrusor overactivity and other urological disorders. In both striated and smooth muscle, botulinum toxin A (BTX-A) is internalized by presynaptic neurons after binding to an extracellular receptor (ganglioside and presumably synaptic vesicle protein 2C). In the neuronal cytosol, BTX-A disrupts fusion of the acetylcholine-containing vesicle with the neuronal wall by cleaving the SNAP-25 protein in the synaptic fusion complex. The net effect is selective paralysis of the low-grade contractions of the unstable detrusor, while still allowing high-grade contraction that initiates micturition. Additionally, BTX-A seems to have effects on afferent nerve activity by modulating the release of ATP in the urothelium, blocking the release of substance P, calcitonin gene-related peptide and glutamate from afferent nerves, and reducing levels of nerve growth factor. These effects on sensory feedback loops might not only help to explain the mechanism of BTX-A in relieving symptoms of overactive bladder, but also suggest a potential role for BTX-A in the relief of hyperalgesia associated with lower urinary tract disorders.

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Urinary Bladder Contraction and Relaxation: Physiology and Pathophysiology

Cited by 786 publications

References 724 publications

A 3D Printed Implantable Device for Voiding the Bladder Using Shape Memory Alloy (SMA) Actuators

A 3D Printed Implantable Device for Voiding the Bladder Using Shape Memory Alloy (SMA) Actuators

Multisystem Neuroprosthetic Training Improves Bladder Function After Severe Spinal Cord Injury

Drug Insight: biological effects of botulinum toxin A in the lower urinary tract

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