Audio LecturePro Feature Storage Phase of Micturition 0:00 / 0:00 1x 0.25x 0.5x 0.75x 1x 1.25x 1.5x 1.75x 2x Micturition is the process of eliminating water and electrolytes from the urinary system, commonly known as urinating. It has two discrete phases: Storage/continence phase when urine is stored in the bladder. Voiding phase where urine is released through the urethra. These phases rely on the coordinated contraction and relaxation of the bladder and urethral sphincters, controlled by the sympathetic, parasympathetic, and somatic nervous systems. In this article, we will discuss the storage phase of micturition, and its regulation and consider some clinical relevance. 3D ModelPro Feature You've Discovered a Pro Feature Access our 3D Model Library Explore, cut, dissect, annotate and manipulate our 3D models to visualise anatomy in a dynamic, interactive way. Learn More Mechanics of Bladder Filling As the bladder fills, applying stress to its folded walls (rugae), the muscular walls relax and distend, increasing the functional capacity of the bladder. This expansion allows pressure within the bladder (intra-vesical pressure) to remain relatively constant over large volume changes. This receptive relaxation (also known as the stress–relaxation phenomenon), is vital to the storage of urine and helps prevent leakage during the storage phase of micturition by ensuring the intra-vesical pressure remains lower than the urethral pressure. Created in BioRender Figure 1Bladder pressure-volume relationship during filling and voiding. During filling, intravesical pressure remains relatively constant due to receptive relaxation. Once a critical volume is reached, the micturition reflex is initiated, leading to voiding. Neural Control of Urinary Storage The pontine continence centre (PCC) controls the storage phase of micturition at the highest level and coordinates the continence centres in the spinal cord. To store urine, the detrusor muscle of the bladder must relax, while both the internal urethral sphincter (IUS) and external urethral sphincter (EUS) contract: The bladder and IUS are under autonomic control meaning they operate unconsciously. The EUS is under somatic control meaning it can be voluntarily opened or closed to control micturition. Bladder Afferent Signalling As the bladder fills, stretch receptors in the detrusor muscle generate low-frequency afferent signals that travel via the pelvic nerve (nerve roots S2-4) to the sacral spinal cord and higher centres in the brain. These signals indicate bladder fullness, but are actively suppressed by higher brain centres to prevent activation of the micturition reflex. Sympathetic Innervation The cerebral cortex sends impulses to the pontine continence centre (PCC), which coordinates detrusor relaxation and sphincter contraction. Descending signals from the PCC activate sympathetic nuclei in the thoracolumbar spinal cord. These sympathetic nuclei use the hypogastric nerve (T10-L2) to release noradrenaline at the bladder causing: Detrusor muscle relaxation via stimulation of β3-adrenoreceptors in the fundus and body of the bladder Internal urethral sphincter (IUS) contraction via stumulation of α1-adrenoreceptors at the bladder neck Note: Simultaneously, parasympathetic outflow via the pelvic nerve (S2–S4) is inhibited, preventing detrusor contraction during bladder filling. Continuous inhibition of the periaqueductal gray (PAG) ensures that afferent input does not activate the pontine micturition centre (PMC). Somatic Innervation Voluntary somatic control of the EUS is achieved via the pudendal nerve (S2-S4), which activates nicotinic cholinergic receptors in the striated muscle of the EUS, causing it to contract. This prevents any urinary leakage through the external sphincter. Created in BioRender Figure 2Diagram summarising the neural pathways involved in the storage of urine in the bladder. Clinical Relevance Urinary Incontinence Urinary incontinence is the inability to store urine effectively, causing leakage of urine. It can arise from various pathological processes and can be broadly grouped into: Stress incontinence – leakage when pressure is exerted on the bladder. This is common in pregnancy and can happen when laughing or sneezing, due to increased intra-abdominal pressure and weakness of the pelvic floor muscles. Urge incontinence – leakage with an intense urge to urinate caused by detrusor muscle overactivity (overactive bladder). This is seen in urinary tract infections (UTIs) and can also be caused by medications, alcohol or caffeine. Mixed incontinence – features of both stress and urge incontinence Overflow incontinence – leakage due to chronic urinary retention caused by bladder outlet obstruction or impaired detrusor contraction. Neurological incontinence – leakage caused by nerve lesions or neurological conditions, such as multiple sclerosis or spinal cord compression Clinical Relevance Neurological Urinary Incontinence Neurological urinary incontinence is caused by lesions to the spinal cord and cerebral centres. Spinal cord injuries are commonly caused by trauma and multiple sclerosis whilst common causes of brain lesions are strokes and brain tumours. Spinal Cord Lesion (Reflex Bladder) Upper motor neurone lesions above S2-4 disrupt sympathetically driven detrusor relaxation and descending inhibition of sacral spinal reflexes from the brain. As the pathways between the bladder and sacral spinal cord remain intact, sensory input from the bladder reaches the sacral cord but not higher centres, causing loss of higher voluntary control. Bladder wall afferent stretch signals are relayed to the disinhibited sacral spinal reflex causing parasympathetic activation and detrusor wall contraction. This phenomenon of involuntary and automatic bladder emptying is known as a reflex bladder. Suprasacral lesions may also cause overactivity of the internal and/or external sphincters, leading to uncoordinated activity with the detrusor, where the sphincters contract instead of relaxing during voiding. This results in detrusor–sphincter dyssynergia, which can prevent complete bladder emptying. Pontine Continence Centre (PCC) Lesions Lesions in the pons can also lead to a complete loss of voiding control and the inability to store urine. Damage to the PCC disrupts coordination of bladder storage and sympathetic outflow, leading to loss of continence. The resultant symptoms are similar to reflex bladder. Other Spinal Lesions Damage to bladder afferent neurones, efferent lower motor neurones or sacral spinal regions disrupt the spinal reflex causing a different spectrum of symptoms. Treatment of Neurological Incontinence Treatment is challenging but there are pharmacological therapies which can be trialled: Anticholinergics (e.g. Oxybutynin, Tolterodine) – reduce parasympathetic input to the bladder. Anticholinergic side effects such as dry mouth and constipation mean they are not used frequently. Oxybutynin in particular should be avoided in frail patients, due to an increased risk of falls. β3-adrenoceptor agonists (e.g. Mirabegron) – relax the detrusor muscle by binding to β3-receptors, increasing its capacity to store urine. These are particularly useful in treating urge urinary incontinence. More invasive therapies include the injection of botulinum toxin A, sacral nerve stimulation, and surgical procedures such as augmentation enterocystoplasty or urinary diversion. Do you think you’re ready? Take the quiz below QuizPro Feature Storage Phase of Micturition Question 1 of 3 Submitting... Skip Next Rate question: You scored 0% Skipped: 0/3 More Questions Available Upgrade to TeachMePhysiology Pro Challenge yourself with over 2100 multiple-choice questions to reinforce learning Learn More Frequent questions What is the storage phase of micturition? The storage phase of micturition is the period when the bladder holds urine, facilitated by the relaxation of the detrusor muscle and contraction of the urethral sphincters. This phase ensures that urine remains in the bladder until it is appropriate to void. How is the storage phase of micturition regulated? The storage phase is regulated by the pontine continence centre, which coordinates the autonomic and somatic nervous systems. The detrusor muscle relaxes while the internal and external urethral sphincters contract to maintain continence. What role do stretch receptors play during bladder filling? Stretch receptors in the detrusor muscle detect bladder fullness and send signals to the sacral spinal cord and brain. These signals help maintain bladder storage by preventing the activation of the micturition reflex until it is appropriate to void. What causes urinary incontinence during the storage phase? Urinary incontinence can occur due to various factors, including stress incontinence from increased abdominal pressure, urge incontinence from detrusor overactivity, and overflow incontinence from bladder outlet obstruction. Each type results in the inability to effectively store urine. How do neurological conditions affect the storage phase of micturition? Neurological conditions can disrupt the control of bladder function, leading to issues such as reflex bladder or detrusor–sphincter dyssynergia. These conditions impair the coordination necessary for effective urine storage and can result in involuntary leakage. Rate This Article