Smooth muscle of the bladder in the normal and the diseased state: Pathophysiology, diagnosis and treatment

The smooth muscle of the normal bladder wall must have some specific properties. It must be very compliant and able to reorganise itself during filling and emptying to accommodate the change in volume without generating any intravesical pressure, but whilst maintaining the normal shape of the bladder. It must be capable of synchronous activation to generate intravesical pressure at any length to allow voiding. The cells achieve this through spontaneous electrical activity combined with poor electrical coupling between cells, and a dense excitatory innervation. In the diseased state, alterations of the smooth muscle may lead to failure to store or failure to empty properly. The diseased states discussed are bladder instability and diabetic neuropathy. Bladder instability is characterised urodynamically by uninhibitable rises in pressure during filling, and is seen idiopathically and in association with bladder outflow obstruction and neuropathy. In diabetic neuropathy, many of the smooth muscle changes are a consequence of diuresis, but there is evidence for alterations in the sensory arm of the micturition reflex. In the unstable bladder, additional alterations of the smooth muscle are seen, which are probably caused by the patchy denervation that occurs. The causes of this denervation are not fully established. Nonsurgical treatment of instability is not yet satisfactory; neuromodulation has some promise, but is expensive, and the mechanisms poorly understood. Pharmacological treatment is largely through muscarinic receptor blockade. Drugs to reduce the excitability of the smooth muscle are being sought, since they may represent a better pharmacological option.