Both the autonomic and voluntary nervous systems normally control storage of urine in the bladder and its subsequent excretion by voiding. Nerves originating locally in the spinal cord control the muscles that keep the exit sphincters closed, sense the buildup of urine and then deactivate the sphincters while stimulating the detrusor muscle in the bladder wall to expel the contents.

This local neural circuit is sufficient to regulate cyclic filling and emptying of the bladder.  After infancy, the local circuit is itself subject to voluntary control by higher levels of the central nervous system which modulate the rhythm in keeping with other activities and social norms. Urinary incontinence, the involuntary loss of urine, results from failure of these mechanisms. Overactive bladder, also called urge incontinence, results from inappropriate contraction of the detrusor muscle that forces urine past the sphincters.

Insufficient closure of the sphincters, a condition called stress incontinence, permits urine flow upon modest increase of the pressure on the exterior of the bladder, such as occurs with coughing or sneezing. In overflow incontinence obstruction of the bladder outflow leads to greatly excessive filling of the bladder, which results in such high pressure that urine leaks past the obstruction. Finally, any condition that interrupts the control of the local neural circuit from the higher central nervous system (e.g., multiple sclerosis, Parkinson›s disease and spinal cord injury) restores the infantile state of automatic voiding upon filling with no voluntary control, a disorder known as neurogenic bladder.

Normal physiological mechanisms of bladder storage and emptying are poorly characterized at the cellular and molecular levels. These include pharmacology, neurophysiology, smooth muscle physiology, striated muscle physiology and urothelial biology. Identifying and characterizing pathophysiological derangements of these mechanisms that produce specific phenotypes may lead to biomarker discovery and a more objective mechanistic basis for diagnosis and descriptions.

Neurological, neuromuscular, inflammatory and neoplastic conditions are among the causes of urinary incontinence, and investigators in all of these fields should be involved in understanding its pathogenesis. Neurophysiological investigation of both central and peripheral nervous mechanisms will be central to our understanding and the deployment of synaptically acting pharmaceuticals.

Other urological conditions, especially benign prostatic hyperplasia and chronic pelvic pain syndromes, undoubtedly impinge on bladder control, and collaborations with practitioners in these areas must be encouraged and supported. Involvement of biomedical engineers should be explored with an eye toward development of implantable devices to control sphincter and detrusor muscles.

Journal of Nephrology and Urology is an Open Access peer-reviewed publication that discusses current research and advancements in diagnosis and management of kidney disorders as well as related epidemiology, pathophysiology and molecular genetics.

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