What is the physiology of the bladder?

Bladder Physiology

Overview of Bladder Function

The bladder functions through two distinct phases—storage and voiding—coordinated by complex interactions between the detrusor muscle, urethral sphincters, and multilevel neural control involving peripheral nerves, spinal cord, and brain centers. 1, 2

Storage Phase Physiology

During urine storage, the bladder outlet remains closed while the detrusor muscle (bladder smooth muscle) stays quiescent and relaxed 1, 2. This phase is maintained through several mechanisms:

• Sympathetic nervous system activation (thoracolumbar outflow) promotes urine storage by increasing urethral resistance and actively depressing detrusor contractions through a spinal vesicosympathetic reflex pathway 3
• Somatic nervous system maintains tonic contraction of the external urethral sphincter (striated muscle) via pudendal nerve innervation 4, 2
• Bladder afferent pathways continuously convey signals of bladder fullness to the central nervous system as the bladder gradually fills at low pressures 2
• Peripheral autonomic ganglia integrate sympathetic and parasympathetic inputs, with facilitatory and inhibitory adrenergic mechanisms modulating efferent neural input to the bladder 3

Voiding Phase Physiology

When bladder volume reaches the micturition threshold and voiding is socially appropriate, a coordinated switch occurs from storage to voiding 2:

• Pontine micturition center (located in the dorsolateral pons) is activated and serves as the primary supraspinal control center initiating bladder emptying 1
• Sacral parasympathetic nerves (pelvic nerves) provide excitatory input to the detrusor muscle through both cholinergic and purinergic neurotransmission 1
• Simultaneous urethral relaxation occurs through nitrergic (nitric oxide-mediated) inhibitory input via the same parasympathetic pathways 1
• External urethral sphincter relaxation results from inhibition of somatic motoneurons in the sacral spinal cord 3

The essential neuronal events are: activation of parasympathetic pathways to the detrusor via a spinobulbospinal pathway, and inhibition of somatic input to the external sphincter through inhibitory mechanisms in the sacral spinal cord 3.

Neural Organization and Coordination

Spinal Level Integration

• Sacral spinal interneurons (located in the region of parasympathetic preganglionic neurons and sphincter motoneurons) mediate both excitatory and inhibitory actions of descending and segmental reflexes 4
• Lumbar-sacral interneuron ensembles orchestrate reciprocity between bladder parasympathetic efferents and external urethral sphincter somatic motoneurons 5
• Segmental sensory information from visceral organs and perineum integrates with supraspinal inputs at the spinal level 4

Supraspinal Control

• Ascending and descending connections between spinal segments and brain regions provide the reflex substrates for normal continence and micturition 4
• Voluntary and autonomic control work together to achieve the complex coordination required for appropriate bladder function 2
• Forebrain and midbrain networks integrate with spinal circuits to determine socially appropriate timing for voiding 5, 2

Pharmacological Targets in Bladder Physiology

Muscarinic Receptors and Detrusor Function

• Antimuscarinic medications (such as oxybutynin and tolterodine) competitively antagonize muscarinic receptors that mediate bladder contraction 6, 7
• Oxybutynin exerts direct antispasmodic effects on bladder smooth muscle, relaxing the detrusor and increasing bladder capacity while diminishing frequency of uninhibited contractions 6
• Tolterodine exhibits high specificity for muscarinic receptors with pronounced effects on bladder function, increasing residual urine volume and decreasing detrusor pressure consistent with antimuscarinic action on the lower urinary tract 7

Clinical Implications of Detrusor Dysfunction

• Detrusor overactivity (48% of diabetic cystopathy cases) results from uninhibited bladder contractions and responds to antimuscarinic therapy 8
• Detrusor underactivity (30% of cases) involves impaired contractility where the tonic phase of bladder emptying is not well sustained, leading to incomplete emptying and elevated post-void residual volumes 9
• Mixed dysfunction can occur when detrusor contractility is impaired alongside overactivity, resulting in urgency, urge incontinence, and incomplete emptying 9

Common Pitfalls in Understanding Bladder Physiology

• Reciprocity between bladder and sphincter is essential: Normal voiding requires coordinated detrusor contraction with simultaneous sphincter relaxation; loss of this coordination (detrusor-sphincter dyssynergia) indicates upper motor neuron dysfunction 9
• Peripheral ganglia are not passive relays: Vesical ganglia contain spontaneously active cells and can modulate efferent neural input, playing an active role in bladder control beyond simple signal transmission 3
• Sexual dimorphism exists: Developmental and anatomical differences between sexes affect lower urinary tract function and should inform treatment approaches 5
• Neuroplasticity occurs with injury: Spinal cord injury seriously damages or eliminates normal voiding ability through pathological changes in neural circuits, not just interruption of pathways 5, 4