Micturition has two discrete phases: the storage/continence phase, when urine is stored in the bladder; and the voiding phase, where urine is released through the urethra. These phases require coordinated contraction/relaxation of the bladder and urethral sphincters, which are all under control of the sympathetic, parasympathetic and somatic nervous systems.
In this article we shall look specifically at the storage phase of micturition and its control, primarily by the sympathetic nervous system.
The storage phase of micturition is controlled at the highest level by continence centres of the brain. These in turn control the continence centres of the spinal cord.
To stimulate storage, impulses from the cerebral cortex travel to the pons of the brainstem. The pons is responsible for coordinating the actions of the urinary sphincters and the bladder, and the area involved in the storage phase is the pontine continence centre (in the L-Region of the pons). From here, signals are sent to the sympathetic nuclei in the spinal cord, and finally to the detrusor muscle and internal urethral sphincter (IUS) of the bladder.
The impulse travels from the spinal cord to the bladder via the sympathetic hypogastric nerve (nerve roots L1-L2). At the bladder, this stimulates:
- Relaxation of the detrusor muscle in the bladder wall – via stimulation of β3-receptors in the fundus and the body of the bladder.
- Contraction of the IUS – via stimulation of α1-receptors at the bladder neck
The external urethral sphincter (EUS) is not controlled by the hypogastric nerve – it is under voluntary somatic control. In the storage phase impulses travel to the EUS via the pudendal nerve (nerve roots S2-S4) to nicotinic receptors on the striated muscle, resulting in contraction of the sphincter.
This coordinated relaxation of the detrusor muscle and contraction of the urethral sphincters allow the bladder to fill with urine, and allow for it to be stored for many hours. As the bladder fills, the folds in the bladder walls (rugae) flatten and the walls distend, increasing the capacity of the bladder. This means that as the bladder fills, it expands, allowing the pressure inside (the intra-vesical pressure) to remain the same and remain lower than urethral pressure – to prevent urine from leaking out. This is known as receptive relaxation.
Clinical Relevance – Incontinence
Spinal Cord Lesion above T12 – Reflex Bladder
In an upper motor neurone lesion, sympathetic input to the bladder is lost, leading to high detrusor pressure. Afferent signals from the bladder are also unable to reach the brain, and so the external urethral sphincter remains constantly relaxed. The parasympathetic system would initiate detrusor wall contraction in response to bladder wall stretch, and so the bladder would automatically empty as it fills – known as a reflex bladder. The causes of such spinal cord injuries include RTAs and Multiple Sclerosis.
Lesion in the Pontine Continence Centre (PCC) – Incontinence
Lesions in the pons can lead to a complete loss of voiding control and the inability to store urine. In damage to the PCC, sympathetic input to the bladder is lost. This results in the same symptoms as a reflex bladder, although the damage is in a different location. Typical causes of such brain lesions are strokes, brain tumours and Parkinsons disease.
Treatment of Incontinence
β3-adrenoceptor agonists (eg. Mirabegron) bind to β3-receptors on the detrusor muscle, and stimulate relaxation of the muscle. Therefore these drugs can be used to increase the bladders capacity to store urine in the treatment of urge urinary incontinence.
Anticholinergics (eg. Oxybutynin) can also be used in incontinence treatment, to reduce parasympathetic input to the bladder. However these are more likely to result in side effects such as a dry mouth or constipation, so are used less frequently.