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Urination

Release of urine from the urinary bladder

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Manneken Pis Brussel
Pbrundel · CC BY-SA 3.0

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Through Urine, Bladder and Urethra

In some animals, in addition to expelling waste material, urination can mark territory or express submissiveness. Physiologically, urination involves coordination between the central, autonomic, and somatic nervous systems. Brain centres that regulate urination include the pontine micturition center, periaqueductal gray, and the cerebral cortex.

Anatomy and physiology

Anatomy of the bladder and outlet

The main organs involved in urination are the urinary bladder and the urethra. The smooth muscle of the bladder, known as the detrusor, is innervated by sympathetic nervous system fibers from the lumbar spinal cord and parasympathetic fibers from the sacral spinal cord. Fibers in the pelvic nerves constitute the main afferent limb of the voiding reflex; the parasympathetic fibers to the bladder that constitute the excitatory efferent limb also travel in these nerves. Part of the urethra is surrounded by the male or female external urethral sphincter, which is innervated by the somatic pudendal nerve originating in the cord, in an area termed Onuf's nucleus.

Smooth muscle bundles pass on either side of the urethra, and these fibers are sometimes called the internal urethral sphincter, although they do not encircle the urethra. Further along the urethra is a sphincter of skeletal muscle, the sphincter of the membranous urethra (external urethral sphincter). The bladder's epithelium is termed transitional epithelium which contains a superficial layer of dome-like cells and multiple layers of stratified cuboidal cells underneath when evacuated. When the bladder is fully distended the superficial cells become squamous (flat) and the stratification of the cuboidal cells is reduced in order to provide lateral stretching.

Physiology

The physiology of micturition and the physiologic basis of its disorders are subjects about which there is much confusion, especially at the supraspinal level. Micturition is fundamentally a spinobulbospinal reflex facilitated and inhibited by higher brain centers such as the pontine micturition center and, like defecation, subject to voluntary facilitation and inhibition.

In healthy individuals, the lower urinary tract has two discrete phases of activity: the storage (or guarding) phase, when urine is stored in the bladder, and the voiding phase, when urine is released through the urethra. The state of the reflex system is dependent on both a conscious signal from the brain and the firing rate of sensory fibers from the bladder and urethra. At low bladder volumes, afferent firing is low, resulting in excitation of the outlet (the sphincter and urethra), and relaxation of the bladder. At high bladder volumes, afferent firing increases, causing a conscious sensation of urinary urge. When an individual consciously initiates voiding, the sphincters relax and the bladder contracts until it empties completely, at which point the bladder relaxes and the outlet contracts to re-initiate storage. The muscles controlling micturition are controlled by the autonomic and somatic nervous systems. During the storage phase, the internal urethral sphincter remains tense and the detrusor muscle relaxed by sympathetic stimulation. During micturition, parasympathetic stimulation causes the detrusor muscle to contract and the internal urethral sphincter to relax. The external urethral sphincter (sphincter urethrae) is under somatic control and is consciously relaxed during micturition.

In infants, voiding occurs involuntarily (as a reflex). The ability to voluntarily inhibit micturition develops by the age of two–three years, as control at higher levels of the central nervous system develops. In the adult, the volume of urine in the bladder that normally initiates a reflex contraction is about 300–400 millilitres (11–14 imp fl oz; 10–14 US fl oz).

Storage phase

During storage, bladder pressure stays low, because of the bladder's highly compliant nature. A plot of bladder (intravesical) pressure against the depressant of fluid in the bladder (called a cystometrogram), will show a very slight rise as the bladder is filled. This phenomenon is a manifestation of the law of Laplace, which states that the pressure in a spherical viscus is equal to twice the wall tension divided by the radius. In the case of the bladder, the tension increases as the organ fills, but so does the radius. Therefore, the pressure increase is slight until the organ is relatively full. The bladder's smooth muscle has some inherent contractile activity; however, when its nerve supply is intact, stretch receptors in the bladder wall initiate a reflex contraction that has a lower threshold than the inherent contractile response of the muscle.

Action potentials carried by sensory neurons from stretch receptors in the urinary bladder wall travel to the sacral segments of the spinal cord through the pelvic nerves. Since bladder wall stretch is low during the storage phase, these afferent neurons fire at low frequencies. Low-frequency afferent signals cause relaxation of the bladder by inhibiting sacral parasympathetic preganglionic neurons and exciting lumbar sympathetic preganglionic neurons. Conversely, afferent input causes contraction of the sphincter through excitation of Onuf's nucleus, and contraction of the bladder neck and urethra through excitation of the sympathetic preganglionic neurons.

Diuresis (production of urine by the kidney) occurs constantly, and as the bladder becomes full, afferent firing increases, yet the micturition reflex can be voluntarily inhibited until it is appropriate to begin voiding.

Voiding phase

Voiding begins when a voluntary signal is sent from the brain to begin urination, and continues until the bladder is empty.

Bladder afferent signals ascend the spinal cord to the periaqueductal gray, where they project both to the pontine micturition center and to the cerebrum. At a certain level of afferent activity, the conscious urge to void or urination urgency, becomes difficult to ignore. Once the voluntary signal to begin voiding has been issued, neurons in the pontine micturition center fire maximally, causing excitation of sacral preganglionic neurons. The firing of these neurons causes the wall of the bladder to contract; as a result, a sudden, sharp rise in intravesical pressure occurs. The pontine micturition center also causes inhibition of Onuf's nucleus, resulting in relaxation of the external urinary sphincter. When the external urinary sphincter is relaxed urine is released from the urinary bladder when the pressure there is great enough to force urine to flow out of the urethra. The micturition reflex normally produces a series of contractions of the urinary bladder.

The flow of urine through the urethra has an overall excitatory role in micturition, which helps sustain voiding until the bladder is empty.

Many men, and some women, may sometimes briefly shiver after or during urination.

After urination, the female urethra empties partially by gravity, with assistance from muscles. Urine remaining in the male urethra is expelled by several contractions of the bulbospongiosus muscle, and, by some men, manual squeezing along the length of the penis to expel the rest of the urine.

For land mammals over a kilogram, the duration of urination does not vary with body mass, being dispersed around an average of 21 seconds (standard deviation 13 seconds), despite a four-order-of-magnitude (1000×) difference in bladder volume. This is due to increased urethra length of large animals, which amplifies gravitational force (hence flow rate), and increased urethra width, which increases flow rate. For smaller mammals a different phenomenon occurs, where urine is discharged as droplets, and urination in smaller mammals, such as mice and rats, can occur in less than a second. The posited benefits of faster voiding are decreased risk of predation (while voiding) and decreased risk of urinary tract infection.

Voluntary control

The mechanism by which voluntary urination is initiated remains unsettled. One possibility is that the voluntary relaxation of the muscles of the pelvic floor causes a sufficient downward tug on the detrusor muscle to initiate its contraction. Another possibility is the excitation or disinhibition of neurons in the pontine micturition center, which causes concurrent contraction of the bladder and relaxation of the sphincter.

There is an inhibitory area for micturition in the midbrain. After transection of the brain stem just above the pons, the threshold is lowered and less bladder filling is required to trigger it, whereas after transection at the top of the midbrain, the threshold for the reflex is essentially normal. There is another facilitatory area in the posterior hypothalamus. In humans with lesions in the superior frontal gyrus, the desire to urinate is reduced and there is also difficulty in stopping micturition once it has commenced. However, stimulation experiments in animals indicate that other cortical areas also affect the process.

The bladder can be made to contract by voluntary facilitation of the spinal voiding reflex when it contains only a few milliliters of urine. Voluntary contraction of the abdominal muscles aids the expulsion of urine by increasing the pressure applied to the urinary bladder wall, but voiding can be initiated without straining even when the bladder is nearly empty. Voiding can also be consciously interrupted once it has begun, through a contraction of the perineal muscles. The external sphincter can be contracted voluntarily, which will prevent urine from passing down the urethra.

Experience of urination

The need to urinate is experienced as an uncomfortable, full feeling. It is highly correlated with the fullness of the bladder. In many males the feeling of the need to urinate can be sensed at the base of the penis as well as the bladder, even though the neural activity associated with a full bladder comes from the bladder itself, and can be felt there as well. In females the need to urinate is felt in the lower abdomen region when the bladder is full. When the bladder becomes too full, the sphincter muscles will involuntarily relax, allowing urine to pass from the bladder. Release of urine is experienced as a lessening of the discomfort.

Disorders

Clinical conditions

Many clinical conditions or urologic diseases can cause disturbances to normal urination, including:

  • Urinary incontinence, the inability to hold urine
    • Stress incontinence, incontinence as a result of external mechanical disturbances
    • Urge incontinence, incontinence that occurs as a result of the uncontrollable urge to urinate
    • Mixed incontinence, a combination of the two types of incontinence
  • Urinary retention, the inability to initiate urination
  • Overactive bladder, a strong urge to urinate, usually accompanied by detrusor overactivity
  • Interstitial cystitis, a condition characterized by urinary frequency, urgency, and pain
  • Prostatitis, an inflammation of the prostate gland that can cause urinary frequency, urgency, and pain
  • Benign prostatic hyperplasia, an enlargement of the prostate that can cause urinary frequency, urgency, retention, and the dribbling of urine
  • Urinary tract infection, which can cause urinary frequency and dysuria
  • Polyuria, abnormally large production of urine, associated with, in particular, diabetes mellitus (types 1 and 2), and diabetes insipidus
  • Oliguria, low urine output, usually due to a problem with the upper urinary tract
  • Anuria refers to absent or almost absent urine output.
  • Micturition syncope, a vasovagal response which may cause fainting.
  • Paruresis, the inability to urinate in the presence of others, such as in a public toilet.
  • Bladder sphincter dyssynergia, a discoordination between the bladder and external urethral sphincter as a result of brain or spinal cord injury

Diuretics are drugs that increase the production of urine, whereas antidiuretics decrease it.

Experimentally induced disorders

There are three major types of bladder dysfunction due to neural lesions: (1) the type due to interruption of the afferent nerves from the bladder; (2) the type due to interruption of both afferent and efferent nerves; and (3) the type due to interruption of facilitatory and inhibitory pathways descending from the brain. In all three types the bladder contracts, but the contractions are generally not sufficient to empty the viscus completely, and residual urine is left in the bladder. Paruresis, also known as shy bladder syndrome, is an example of a bladder interruption from the brain that often causes total interruption until the person has left a public area. These people (males) may have difficulty urinating in the presence of others and will consequently avoid using urinals without dividers or those directly adjacent to another person. Alternatively, they may opt for the privacy of a stall or simply avoid public toilets altogether.

Deafferentation

When the sacral dorsal roots are cut in experimental animals or interrupted by diseases of the dorsal roots such as tabes dorsalis in humans, all reflex contractions of the bladder are abolished. The bladder becomes distended, thin-walled, and hypotonic, but there are some contractions because of the intrinsic response of the smooth muscle to stretch.

Denervation

When the afferent and efferent nerves are both destroyed, as they may be by tumors of the cauda equina or filum terminale, the bladder is flaccid and distended for a while. Gradually, however, the muscle of the "decentralized bladder" becomes active, with many contraction waves that expel dribbles of urine out of the urethra. The bladder becomes shrunken and the bladder wall hypertrophied. The reason for the difference between the small, hypertrophic bladder seen in this condition and the distended, hypotonic bladder seen when only the afferent nerves are interrupted is not known. The hyperactive state in the former condition suggests the development of denervation hypersensitization even though the neurons interrupted are preganglionic rather than postganglionic.

Spinal cord injury

During spinal shock, the bladder is flaccid and unresponsive. It becomes overfilled, and urine dribbles through the sphincters (overflow incontinence). After spinal shock has passed, a spinally mediated voiding reflex ensues, although there is no voluntary control and no inhibition or facilitation from higher centers. Some paraplegic patients train themselves to initiate voiding by pinching or stroking their thighs, provoking a mild mass reflex. In some instances, the voiding reflex becomes hyperactive. Bladder capacity is reduced and the wall becomes hypertrophied. This type of bladder is sometimes called the spastic neurogenic bladder. The reflex hyperactivity is made worse, and may be caused, by infection in the bladder wall.

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