Voiding Phase of Micturition

Written by Joe Reynolds and Asad Hashmi

Last updated 6th May 2026
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The bladder (detrusor muscle) stores urine and controls urination to occur at an appropriate time. Urination is the process of excreting this stored urine from the urinary bladder. It is also known as the voiding phase of micturition. The ability to voluntarily control micturition develops from 2 years as the CNS develops.

In this article we will look at the steps of micturition (urination) and its clinical relevance.

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Volumes in Micturition

Whilst the capacity of the bladder varies from roughly 300-550ml, afferent nerves in the bladder wall signal the need to void the bladder at around 400ml of filling. Micturition itself is typically a short-lasting event.

Urinary flow rate in a full bladder is:

  • 20-25ml/s in men
  • 25-30ml/s in women

After a successful voluntary void, a normal healthy adult may retain about 50 mL of urine (post-void residual).

Neural Control of Micturition

The passing of urine is under unconscious parasympathetic control via a spinal reflex which undergoes remodelling during childhood, allowing it to be overridden at various control points by higher voluntary somatic control.

For micturition to occur the detrusor muscle must contract while the internal (only present in males) and external urethral sphincters relax concomitantly.

Primitive Micturition Reflex

As the bladder reaches capacity, stretch receptors in the detrusor muscle are intensely activated and bladder afferents send signals via the pelvic nerve (nerve roots S2-4) to the spinal cord. Efferent signals are sent back to the detrusor via parasympathetic fibres in the pelvic nerve, releasing acetylcholine (ACh) at the neuromuscular interface.

Ach acts on muscarinic ACh receptors (M3 receptors) on the detrusor muscle, causing contraction and increased intra-vesicular pressure. This is the micturition reflex.

After 2 years of age, following extensive remodelling, voluntary control of this reflex arc is gained by higher centres. Instead of synapsing in the spinal cord, information from bladder afferents ascend via the spinal cord to the periaqueductal gray in the midbrain, to the pontine micturition centre (PMC) and cerebral cortex.

Though the PMC now stimulates the efferent limb of this reflex, the primitive spinal reflex is still relevant in pathological states.

Control by Higher Centres

Higher brain centres can voluntarily inhibit or facilitate the micturition reflex, primarily via the PMC. The PMC and micturition reflex is normally inhibited by higher centres until the decision to urinate is made.

Upon the voluntary decision to urinate, inhibition of the PMC is released. This allows the PMC to stimulate the sacral preganglionic parasympathetic neurons, causing detrusor contraction.

The PMC also suppresses Onuf’s nucleus in the sacral spinal cord, reducing the somatic activity of the pudendal nerve (S2–S4) and voluntary contraction of the external urethral sphincter. This causes relaxation of the external urethral sphincter.

Simultaneously, in response to bladder afferents from a full bladder, the PMC also reduces sympathetic stimulation of the hypogastric nerve (T10-L2), allowing relaxation of the internal urethral sphincter. This allows the urethra to distend, enabling the passage of urine.

Bladder Emptying

Once micturition has begun, bladder contractions lead to increased stimulation of afferents and increased contraction in a positive feedback and self-regenerating process. This ensures bladder emptying.

In the female, urination is assisted by gravity, while in the male, bulbospongiosus muscle contractions along the length of the penis also helps to expel all of the urine.

Visual depiction of bladder and the role of the pelvic, hypogastric and pudendal nerves in its voiding during micturition.

Figure 1
Diagram summarising the neural pathways involved in voiding.

Clinical Relevance

Urinary Retention

Urinary retention is the inability to voluntarily empty the urinary bladder, resulting in incomplete or absent voiding. This may result from mechanical obstruction, neural dysfunction, or pharmacological effects.

Damage to parasympathetic pathways (S2–S4) or inhibition of muscarinic (M₃) receptors reduces detrusor contractility. This means intravesicular pressure cannot overcome urethral resistance, preventing adequate emptying.

Persistent contraction or obstruction of the EUS or IUS, increases outlet resistance, preventing urine outflow despite normal detrusor activity.

Lesions of the higher control centres can impair coordination through inhibition of the micturition reflex or the inability to initiate voiding.

Reduced detrusor contractility Increased outlet resistance Impaired coordination
Diabetic autonomic neuropathy Benign prostatic hyperplasia Stroke
Spinal cord injury affecting sacral pathways Constipation Parkinson’s
Anticholinergic drug use Strictures Multiple sclerosis
Urethral tumours

Benign prostatic hyperplasia is the most common cause of retention in men

Clinical Features

Urinary retention can present with abdominal pain or discomfort, an inability to urinate despite urinary urgency or suprapubic distension.

Management and Complications

In an acute setting, treatment includes urinary catheterisation, prostatic stenting, or a suprapubic cystostomy.

Long-term treatment is dependent on the cause. BPH can be managed pharmacologically through drugs such as alpha-blockers e.g. tamsulosin or 5-alpha-reductase inhibitors e.g. finasteride. Alternatively, if indicated, it can also be surgically treated through prostatectomy or transurethral prostatic resection.

Complications include:

  • Urinary incontinence
  • Nocturia (the need to urinate at night)
  • Hydronephrosis – high pressure in the bladder can push urine back up ureters into the kidneys. This causes the renal pelvises to expand
  • Kidney failure
  • Recurrent urinary tract infections
  • Bladder rupture – retention can lead to anuria (inability to pass urine). This can cause the bladder to stretch and possibly tear

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