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Physiology · Excretion

Urination

Micturition

Urination is a complex physiological process of bladder emptying that ensures the removal of metabolic waste products from the body. It consists of two main stages: urine storage and its subsequent elimination, which is strictly controlled by spinal and cortical centers of the nervous system.

Call threshold volumeThe urination threshold is reached at a volume of 150–300 ml of urine.
PressureDuring critical stretching, the hydrostatic pressure rises to 15 mm Hg.
Residual volumeNormally, about 50 ml of urine remains after the act of urination.
5 min readFor medical studentsUpdated 09/24/2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Mechanisms of urine retention

Urine accumulation in the bladder is possible due to the tonic contraction of two sphincters that close off the urethra.

  • The internal sphincter of the urinary bladder is formed by smooth muscle fibers. Its tone is maintained by the sympathetic nervous system (centers are located in the lumbar segments $L_1-L_2$). Impulses pass through the hypogastric plexus ganglion, ensuring compression.
  • The external sphincter of the urethra consists of striated muscle and is subject to voluntary control. Somatic innervation originates from the sacral segments of the spinal cord ($S_2-S_4$) via the pudendal nerve (n. pudendus).

Filling of the bladder with urine arriving in portions from the ureters occurs without a sharp increase in wall tone due to its elasticity.

Formation of the urge and cortical control

During bladder filling, the stretching of its walls activates mechanoreceptors (and partially chemoreceptors). Afferent impulses are generated, which are transmitted to the spinal cord, and then to subcortical structures and the cerebral cortex, forming the urge to urinate.

An important role in preventing premature emptying is played by reflex inhibition at the spinal cord level. Activation of inhibitory neurons involving GABA suppresses parasympathetic activity, preventing the bladder muscle (detrusor) from contracting.

The cerebral cortex provides conscious control over the process. When an urge occurs, the situation is assessed. If conditions are unfavorable, the cortex suppresses the spinal centers via the pyramidal tract, and a temporary delay in urination occurs.

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Emptying phase

When conditions allow, the inhibitory influence of the cortex on the spinal cord is lifted, and the involuntary emptying mechanism is triggered, coordinated by the parasympathetic center in the sacral segments ($S_2-S_4$).

  1. Excitement along the pelvic nerve (n. pelvicus) causes contraction of the bladder wall (detrusor).
  2. Simultaneously, inhibitory interneurons of the spinal cord are activated, leading to the cessation of impulses along the somatic pudendal nerve.
  3. Relaxation of the external sphincter occurs, while the internal sphincter opens reflexively upon contraction of the detrusor.

As a result, urine is expelled through the urethra under pressure. This complex process is part of the general functional system of urination, where the system-forming factor is the bladder filling volume.

Ureteral urodynamics

The transport of urine from the renal pelves to the bladder is not just a slow peristalsis. Urine moves in "columns" with a volume of about 10 ml. Movement occurs with acceleration: slower in the initial parts of the ureter and faster near the bladder.

The flow rate depends on retroperitoneal pressure, and the frequency of portions is determined by the hydrostatic pressure in the pelves. Local autoregulation maintains this pressure at a constant level. The anatomical insertion of the ureters into the bladder at an acute angle prevents the backflow of urine (reflux) during bladder filling.

Briefly: answers to topical questions

What neurotransmitters and receptors mediate detrusor contraction upon activation of the parasympathetic system?

According to the provided sources, the neurotransmitter of parasympathetic innervation is acetylcholine. Information about specific efferent receptors of the detrusor is not provided in the texts.

  • Acetylcholine is released by the second neurons of the parasympathetic system.
  • Parasympathetic impulses to the bladder travel via the pelvic nerve (n. pelvicus) from the sacral segments S2–S4.
  • Effect of parasympathetic activation: contraction of the detrusor/bladder wall and an increase in intravesical pressure.
  • Stretch mechanoreceptors and chemoreceptors mentioned in the sources belong to the afferent link of urge formation, rather than to specific efferent receptors of the detrusor.

In which specific area of the cerebral cortex is the highest center for urination control located?

The sources do not single out a single "highest center" of urination in the cortex. The paracentral lobule is indicated as a specific cortical area.

  • The urination center is located in the reticular formation of the brainstem near the locus coeruleus.
  • From this center, impulses enter the paracentral lobule on the medial surface of the cerebral hemispheres, as well as into other brain regions.
  • Area 4 of the paracentral lobule indicates the cortical representation of the bladder, foot, and rectum.
  • Suprasegmental inhibitory influence on the pontine micturition center is associated with the frontal lobe cortex, cingulate gyrus, paracentral lobule, and basal ganglia.

What happens to the function of urination in a complete transection of the spinal cord above the sacral segments?

With a complete transverse spinal cord lesion above the sacral segments, voluntary control of urination is lost. Changes are described in stages:

  • In the acute period, during the stage of spinal shock, the reflex activity of the spinal cord is suppressed, detrusor paresis develops, and the residual tone of the urethral sphincters is preserved; the consequence is urinary retention/acute urinary retention.
  • In the subacute stage, acute retention can be replaced by paradoxical ischuria: urine is released drop by drop or in small portions from an overdistended bladder.
  • After a few weeks, segmental reflex functions are restored and an automatic or reflex bladder is formed: upon filling, automatic contraction of the detrusor and relaxation of the sphincters occur with the release of urine.
  • With a lesion above the sacral segments, detrusor hyperreflexia may develop. Detrusor-sphincter dyssynergia is defined as involuntary contraction of the detrusor without relaxation of the external sphincter and can lead to urinary retention and increased frequency of reflex urination.

Class and exam questions

Which nervous system predominates during urine accumulation?

During the storage phase, the sympathetic nervous system dominates (compressing the internal sphincter) and somatic control (maintaining the tone of the external sphincter).

What happens when the connection between the brain and spinal cord is disrupted?

Conscious cortical control is lost. Urination begins to occur involuntarily as the bladder fills due to autonomous spinal reflexes.

How does the parasympathetic system act during the act of urination?

It causes contraction of the smooth muscles of the bladder wall (detrusor) and promotes relaxation of the internal sphincter, ensuring the expulsion of urine.

What will happen with prolonged urinary retention?

In addition to pronounced discomfort, partial reabsorption of the bladder contents back into the blood and slight concentration of urine may occur.

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What else to study on this topic

  • The role of the hypothalamus in the autonomic regulation of water-salt balance
  • Hormonal regulation of the rate of urine formation
  • Mechanisms of conditioned reflex control formation in ontogenesis
  • Physiology of spinal shock and automatic bladder syndrome
  • Chemoreception of the bladder wall and its role

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