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Related Concept Videos

The Micturition Reflex01:26

The Micturition Reflex

Urination, or micturition involves the coordination of the bladder's detrusor muscle and two sphincters to ensure controlled bladder emptying.
The process begins with bladder filling, where the bladder wall stretches as urine accumulates. This stretching activates the urine storage reflex, mediated by the sacral spinal segments and the pontine storage center. Efferent sympathetic impulses stimulate the detrusor muscle to relax and the internal urethral sphincter to contract, facilitating urine...
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The urinary bladder is a hollow, muscular sac that temporarily stores urine before it is expelled from the body. It can hold approximately 600 mL of urine prior to micturition. The bladder is retroperitoneal and located behind the pubic symphysis in the pelvic floor.
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Urinary Bladder Distention Evoked Visceromotor Responses as a Model for Bladder Pain in Mice
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Urinary bladder function and somatic sensitivity in vasoactive intestinal polypeptide (VIP)-/- mice.

Simon Studeny1, Bopaiah P Cheppudira, Susan Meyers

  • 1Department of Neurology, University of Vermont College of Medicine, D415A Given Research Building, Burlington, VT 05405, USA.

Journal of Molecular Neuroscience : MN
|June 19, 2008
PubMed
Summary
This summary is machine-generated.

Mice lacking vasoactive intestinal polypeptide (VIP) showed altered bladder function and increased sensitivity. This suggests VIP plays a crucial role in regulating bladder activity and inflammation.

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Area of Science:

  • Neuroscience
  • Urology
  • Immunology

Background:

  • Vasoactive intestinal polypeptide (VIP) is an immunomodulatory neuropeptide involved in micturition regulation.
  • VIP also possesses endogenous anti-inflammatory properties, making it a potential therapeutic target for inflammatory conditions.

Purpose of the Study:

  • To investigate the role of VIP in urinary bladder function and somatic sensitivity.
  • To determine the impact of VIP deficiency on bladder inflammation and associated pain.

Main Methods:

  • Comparison of bladder function and sensitivity between VIP-deficient (VIP(-/-)) mice and wildtype (WT) controls.
  • Assessment of bladder voiding parameters using cystometry.
  • Evaluation of bladder permeability and inflammatory responses following cyclophosphamide administration.

Main Results:

  • VIP(-/-) mice exhibited increased bladder mass, larger urine spots, increased void volumes, and shorter intercontraction intervals.
  • A significant increase in urea permeability was observed in VIP(-/-) mice.
  • VIP deficiency led to exaggerated bladder hyperreflexia and prolonged hindpaw and pelvic sensitivity upon induction of inflammation.

Conclusions:

  • VIP deficiency significantly impacts urinary bladder function, leading to alterations in voiding dynamics and increased urea permeability.
  • The absence of VIP exacerbates bladder inflammation-induced hyperreflexia and somatic hypersensitivity.
  • These findings highlight VIP's critical role in modulating the neural control of micturition and inflammatory responses within the urinary bladder.