Victor Forge
The detrusor muscle, also known as the detrusor urinae muscle, is a smooth muscle found in the wall of the bladder. It contracts during urination to release urine and remains relaxed to allow the bladder to store urine. The detrusor muscle is innervated by the autonomic nervous system, which controls the complex micturition process. The external urinary sphincter is under voluntary control and is located more distally than the internal sphincter. Normal micturition is a voluntary act, but in cases of overactive bladder (OAB), the detrusor muscle contracts out of a person's control, resulting in involuntary contractions known as detrusor overactivity.
| Characteristics | Values |
|---|---|
| Definition | The detrusor muscle, also detrusor urinae muscle, is the muscularis propria of the urinary bladder and is a smooth muscle found in the wall of the bladder. |
| Structure | The detrusor muscle is an interlacing network of multi-directional smooth muscle fibres that produce a trabeculated appearance on gross inspection. |
| Function | The detrusor muscle contracts during voiding events to expel urine from the bladder into the urethra. |
| Innervation | The detrusor muscle is innervated by the autonomic nervous system. During urination, parasympathetic pelvic splanchnic nerves cause contraction of the detrusor muscle. At other times, the muscle is kept relaxed via sympathetic branches from the inferior hypogastric plexus to allow the bladder to fill. |
| Disorders | Detrusor overactivity (DO) and detrusor sphincter dyssynergia (DSD) are two disorders associated with the detrusor muscle. DO is characterised by involuntary contractions of the detrusor muscle, while DSD occurs due to detrusor muscle contraction with concomitant involuntary urethral sphincter contraction. |
Explore related products
What You'll Learn
The detrusor muscle is a smooth muscle
The detrusor muscle, also known as the detrusor urinae muscle or muscularis propria of the urinary bladder, is a smooth muscle found in the bladder wall. It is composed of interlacing muscle fibres that run in multiple directions, forming a trabeculated appearance. This muscle is responsible for maintaining urinary continence and plays a crucial role in the process of micturition (urination).
During the storage phase, the detrusor muscle remains relaxed, allowing the bladder to fill with urine. This relaxation is facilitated by sympathetic branches from the inferior hypogastric plexus. When the bladder is full, nerve signals are sent to the brain via the spinal cord, indicating the urge to urinate. The brain then sends messages back to the bladder, coordinating the contraction of the detrusor muscle and relaxation of the sphincter muscles, enabling the release of urine.
The detrusor muscle contracts during the voiding phase to expel urine from the bladder into the urethra. This contraction increases intravesical pressure, forcing urine through the bladder neck and into the urethra. The coordination between the detrusor muscle and sphincter muscles is essential for normal micturition. Any dysfunction in this coordination can lead to conditions like detrusor sphincter dyssynergia (DSD), characterised by involuntary urethral sphincter contractions during detrusor contractions.
The detrusor muscle is innervated by the autonomic nervous system. Parasympathetic pelvic splanchnic nerves stimulate the contraction of the detrusor muscle during urination. On the other hand, sympathetic innervation inhibits detrusor activity and activates the smooth muscle sphincter, providing involuntary tonic resistance to maintain urinary continence.
In certain conditions, such as overactive bladder (OAB), the detrusor muscle exhibits involuntary contractions, resulting in symptoms like urgency, frequency, and nocturia. This occurs due to excessive nerve signalling to and from the bladder muscle, causing it to contract even when the bladder is not full. Understanding the physiology of the detrusor muscle and its interactions with the nervous system is crucial for managing urinary disorders and ensuring normal urinary function.
Increasing Penis Muscle: A Comprehensive Guide to Maximizing Growth
You may want to see also
Explore related products
It contracts during urination
The detrusor muscle is a smooth muscle that forms the wall of the bladder. It is composed of interlacing muscle fibres that run in different directions, forming three distinct layers. The detrusor muscle is responsible for contracting during urination to release urine from the bladder.
During the storage phase, the bladder fills with urine, and the detrusor muscle remains relaxed to allow for this filling process. The internal urinary sphincter, an extension of the detrusor muscle, surrounds the bladder neck to retain the urine inside. This process is regulated by sympathetic activation, which causes the contraction of the internal sphincter and closes the bladder neck.
When an individual is ready to urinate, nerve signals are sent to the bladder, indicating that it is full. The brain then sends a message to the bladder to contract the detrusor muscle and relax the sphincter muscles, allowing for voiding. This coordination between the detrusor muscle and sphincter muscles is essential for normal urinary function and continence.
During urination, the detrusor muscle contracts to increase intravesical pressure and pull open the bladder neck, forcing urine into the urethra. The external urinary sphincter, located distally from the internal sphincter, is under voluntary control and functions to control the flow of urine. It relaxes during urination to allow urine to flow out of the bladder.
In some cases, such as overactive bladder (OAB) or detrusor overactivity, the detrusor muscle may contract involuntarily, even when the bladder is not full. This can lead to symptoms like urgency, frequency, and nocturia. Additionally, in older adults, the detrusor muscle may cause issues in voiding the bladder, resulting in uncomfortable urinary retention.
Building Muscle Strength: Unlocking the Power Within
You may want to see also
Explore related products
It is innervated by the autonomic nervous system
The detrusor muscle is innervated by the autonomic nervous system. This means that the detrusor muscle is controlled by the autonomic nervous system, which is responsible for regulating involuntary bodily functions. The autonomic nervous system is made up of two main components: the sympathetic nervous system and the parasympathetic nervous system. During the storage phase, when the bladder is filling with urine, the sympathetic nervous system is active. This keeps the detrusor muscle relaxed, allowing the bladder to expand and fill with urine. At the same time, the internal sphincter muscle, which surrounds the neck of the bladder, contracts to keep the urine inside.
When the bladder becomes full, nerve endings in the bladder wall send a message to the brain via the spinal cord. The brain then sends a message back to the bladder to contract the detrusor muscle and relax the sphincter muscles, initiating the voiding phase. This is done under a person's control and is considered a voluntary action. However, in some cases, such as in patients with detrusor overactivity (DO) or detrusor sphincter dyssynergia (DSD), the detrusor muscle may contract involuntarily, causing accidental voiding or incontinence.
During the voiding phase, the parasympathetic nervous system is active. It acts on postganglionic M3 receptors to cause contraction of the detrusor muscle, helping to expel urine from the bladder. The external sphincter muscle, located more distally than the internal sphincter, is also under voluntary control. It functions through pudendal nerve fibres and is situated in the Onuf's nucleus between the S2 and S4 segments of the spinal cord. The coordination between the detrusor contraction and the relaxation of the internal and external sphincters is essential for normal urinary continence and micturition.
The central nervous system, which includes the brain and spinal cord, plays a crucial role in controlling the complex micturition process. It coordinates the activity of the autonomic and somatic nervous systems to ensure normal urinary function. However, spinal cord injuries or lesions can disrupt this process, leading to either a "floppy" (flaccid) bladder or a hyperactive" (spastic or reflex) bladder. A floppy bladder loses detrusor muscle tone and cannot contract for emptying, while a hyperactive bladder may have increased detrusor muscle tone, resulting in involuntary contractions and incontinence.
Strengthen Your Body: Strategies to Counter Weak Muscles
You may want to see also
Explore related products
Detrusor overactivity (DO) is linked to OAB
The detrusor muscle is an interlacing network of multidirectional smooth muscle fibres that form the wall of the bladder. It is innervated by the autonomic nervous system. During urination, the detrusor muscle contracts to release urine from the bladder. At other times, the muscle is kept relaxed to allow the bladder to store urine.
Detrusor overactivity (DO) is characterised by phasic increases in detrusor pressure. It is associated with a range of factors, including ageing, bladder outlet obstruction, psychological stress, and obesity, which cause changes in bladder smooth muscle, neuronal and urothelial function. These factors are also linked to the development of overactive bladder (OAB), a syndrome consisting of urinary urgency, with or without urgency urinary incontinence, and usually accompanied by urinary frequency and nocturia.
The link between DO and OAB is supported by clinical and experimental evidence. For instance, a study by Gillespie and colleagues identified two distinct types of detrusor muscle activity: phasic activity and global contractions. Furthermore, almost a quarter of patients with OAB and urge incontinence do not demonstrate DO on urodynamic testing, while a similar proportion of asymptomatic individuals exhibit DO. This suggests that DO may not be the sole cause of OAB.
The pathophysiological mechanisms underlying the development of OAB and DO involve reduced bladder blood flow, leading to local tissue inflammation, cytokine release, and enhanced oxidative stress. These processes result in altered detrusor sensitivity, detrusor hypertrophy, and fibrosis, as well as afferent hypersensitivity. These mechanisms explain the symptoms of urgency and frequency observed in individuals with OAB.
In summary, DO is linked to OAB through shared risk factors and pathophysiological mechanisms. While DO is often associated with OAB, it is not universally present in all cases of OAB, indicating that other factors may also contribute to the development of OAB.
Kali Muscle: Unlocking the Secrets of His Superhuman Strength
You may want to see also
Explore related products
Detrusor sphincter dyssynergia (DSD) is linked to lower urinary tract symptoms
The detrusor muscle is a smooth muscle found in the wall of the bladder. It remains relaxed to allow the bladder to store urine and contracts during urination to release urine. The detrusor muscle is innervated by the autonomic nervous system. During urination, the parasympathetic pelvic splanchnic nerves cause the detrusor muscle to contract. At other times, the muscle is kept relaxed via sympathetic branches from the inferior hypogastric plexus to allow the bladder to fill.
Detrusor sphincter dyssynergia (DSD) is a condition that causes lower urinary tract symptoms. It is characterised by detrusor muscle contraction with involuntary urethral sphincter activation. This results in bladder outlet obstruction. DSD is associated with neurological conditions such as spinal cord injury, multiple sclerosis, and spina bifida. It is diagnosed during the voiding phase of urodynamic studies using EMG recordings and voiding cystourethrograms.
DSD can be classified into three types: Type 1 is characterised by simultaneous detrusor contraction and sphincter tightening, followed by a decrease in detrusor pressure to allow urination. Type 2 is characterised by clonic contractions during voiding, causing an intermittent urinary stream. Type 3 is characterised by continuous sphincter activity during detrusor contraction, resulting in an inability to void per urethra.
The treatment of DSD includes both pharmacological and non-pharmacological strategies. Transurethral botulinum toxin injection has shown temporary efficacy in reducing symptoms. Other surgical procedures such as sphincterotomy, which weakens the bladder neck and sphincter muscle to facilitate urine flow, may also be considered.
The detrusor muscle plays a crucial role in maintaining urinary function and continence. Its coordination with the urethral sphincter muscles is essential for normal micturition, which consists of a storage phase and a voiding phase. During the storage phase, the bladder fills with urine, while during the voiding phase, the detrusor muscle contracts and the sphincter muscles relax to allow urine to flow out of the bladder.
Muscles' Electric Spark: Voltage Generation Explained
You may want to see also
Frequently asked questions
The detrusor muscle, also known as the detrusor urinae muscle, is a smooth muscle found in the wall of the bladder. It is made up of interlacing multi-directional muscle fibres that form three layers.
The detrusor muscle contracts during urination to release urine. It is innervated by the autonomic nervous system. During urination, nerves act on receptors to cause the detrusor muscle to contract. At other times, the muscle is kept relaxed to allow the bladder to fill.
The detrusor muscle is the muscularis propria component of the bladder. Its primary function is to contract during urination to expel urine from the bladder into the urethra.
The detrusor muscle is normally under voluntary control. However, in certain conditions such as overactive bladder (OAB) or detrusor overactivity, the detrusor muscle may contract involuntarily, even when the bladder is not full.
If the detrusor muscle is not functioning properly, it can lead to issues with voiding the bladder, such as incontinence or urinary retention. Detrusor sphincter dyssynergia (DSD) is a condition where the detrusor muscle contracts involuntarily with inappropriate urethral sphincter contraction, leading to elevated bladder pressures and various types of dysfunctional voiding.
