New Approaches in the Treatment of Overactive Bladder: Targeting Adrenergic Receptors and Neurokinin Receptors

Bladder outlet obstruction, such as benign prostatic hypertrophy, and neurogenic bladder with cerebro-vascular disease and Parkinson's disease, not only cause difficulty in urination, but also overactive bladder. This overactive condition is currently a major health concern, in terms of quality of life. Bladder outlet obstruction leads to bladder hypertrophy, and changes in the nervous control of micturition. Hypertrophied detrusor muscles release nerve growth factor, which also leads to changes in nervous control of micturition, especially sympathetic nerve and c-fiber mediated control. Adrenergic receptors comprise certain subtypes, α1A, α1B, α1D, α2A, α2B, α2D, β1, β2, β3. Recently, α1D and b3 receptors are of particular interest with regard to their functional role in overactive bladder. Tachykinins are the main neuropeptides of c-fiber mediated nervous control. Normally, this c-fiber is silent, however, in pathological conditions, such as bladder outlet obstruction and neurogenic bladder, it becomes activated and causes overactive bladder. Recently, antagonists of tachykinin receptors, neurokinin (NK) 1, 2, 3, have become of interest in regard to their role in the treatment of overactive bladder.This review describes some of the changes in adrenergic and NK receptors in the central nervous system and the spinal micturition center in the overactive bladder, and a new approach to treatment that targets these receptors.