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Related Concept Videos

The Micturition Reflex01:26

The Micturition Reflex

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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...
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Urinary Bladder01:23

Urinary Bladder

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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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Ureters01:22

Ureters

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The ureters are retroperitoneal tubes located on either side of the vertebral column. They are responsible for transporting urine from each kidney to the urinary bladder. These tubes have thick walls and are approximately 25-30 cm long. Their diameter is around 10 mm at the renal pelvis, gradually narrowing to 1 mm as the ureter obliquely enters the posterior bladder wall through the ureteric orifices. The shape of these orifices is slit-like, which helps to prevent urine backflow toward the...
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Disorders of the Urinary System01:20

Disorders of the Urinary System

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The urinary system is responsible for eliminating waste and excess fluids from the body. However, disorders of the urinary system can arise due to various reasons like infections, stress, age, congenital abnormalities, and lifestyle.
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Formation of Concentrated Urine01:23

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There is a gradient of solutes in the interstitial fluid from the renal cortex through the medulla, known as the medullary osmotic gradient. The juxtamedullary nephrons establish and maintain this gradient using countercurrent mechanisms with loops extending deep into the medulla. These nephrons also use countercurrent mechanisms to regulate urine volume and concentration. The interaction between the descending and ascending limbs of the nephron loop creates an osmotic gradient through...
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The early phase of the DCT manages the reabsorption of approximately 10-15% of filtered water, 5–10% of filtered sodium, and 5–10% of filtered chloride. This process is facilitated by Na+–Cl− symporters in apical membranes and sodium-potassium pumps, as well as Cl− leakage channels in basolateral membranes. The early DCT also stands out as a site where parathyroid hormone (PTH) stimulates calcium reabsorption, depending on the body's requirements.
The distal...
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Contractions of ex-vivo mouse bladder driven by activation of channelrhodopsin-2 expressed in urothelial cells.

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Related Experiment Video

Updated: May 27, 2025

A Decentralized Ex Vivo Murine Bladder Model with the Detrusor Muscle Removed for Direct Access to the Suburothelium during Bladder Filling
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Local urothelial cell-driven detrusor contractions.

Firoj Alom, Kyle Joseph Ratcliff, Aaron D Mickle

    Biorxiv : the Preprint Server for Biology
    |February 20, 2025
    PubMed
    Summary

    Urothelial cells release factors that cause local bladder contractions, independent of the nervous system. Optogenetics confirmed this urothelial cell-mediated pathway, highlighting a new mechanism for bladder control.

    Area of Science:

    • Urology
    • Cell Biology
    • Physiology

    Background:

    • Urothelial cells release signaling molecules affecting bladder function.
    • Mechanical stretch of the urothelium is known to trigger neuronal signaling.
    • A local urothelial cell-mediated contraction pathway is theorized but not fully understood.

    Purpose of the Study:

    • To investigate urothelial cell-released signaling molecules' influence on local bladder contractions.
    • To use optogenetics to stimulate urothelial cells and observe their effect on bladder contractions.
    • To elucidate the signaling pathways involved in urothelial cell-mediated bladder contractions.

    Main Methods:

    • Utilized an ex-vivo whole bladder preparation.
    • Stimulated urothelial cells via optogenetics by activating channelrhodopsin-2 (ChR2) with blue light.

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  • Administered various antagonists and inhibitors (PPADS, atropine, nifedipine, YM-254890, carbenoxolone disodium, brefeldin A) to probe signaling pathways.

    • Main Results:

    • Optogenetic stimulation of urothelial cells initiated local bladder contractions.
    • P2X receptor antagonist PPADS and muscarinic antagonist atropine significantly inhibited contractions.
    • Extracellular Ca2+ entry blocker nifedipine abolished contractions, as did G protein-coupled receptor inhibitor YM-254890.
    • Hemichannel inhibitor carbenoxolone disodium and exocytotic pathway inhibitor brefeldin A also significantly inhibited contractions.

    Conclusions:

    • Validated the hypothesis that urothelial release factors can induce local bladder contractions.
    • Demonstrated a urothelial cell-mediated pathway for bladder contraction independent of central nervous system signaling.
    • Further research is needed to determine the clinical relevance in bladder physiology and pathology.