Bladder Function in Experimental Outlet Obstruction: Pharmacologic Responses to Alterations in Innervation, Energetics, Calcium Mobilization, and Genetics

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Abstract
Micturition is a complex neuromuscular process1–3. Although control mechanisms have been identified at several levels of the central nervous system, the final pathway for micturition control is the autonomic innervation of the urinary bladder and related structures. Based on current experimental studies, the bladder’s progressive response to partial outlet obstruction can be divided into three distinct phases: 1) An initial response to surgical induction of partial outlet obstruction. During this phase there are substantial alterations in bladder mass, pharmacology, and physiology. 2) Compensated bladder function immediately follows the “initial phase” and lasts an indefinite, variable period of time. This period is characterized by relatively stable bladder mass, and stable contractile responses (which may be above control values) to field, bethanechol, and KCl stimulation. 3) Finally, at some point, functional ability to empty degenerates and the bladder becomes “decompensated”. The decompensated phase is characterized by progressive deterioration in contractile and functional status, a rapid increase in mass, and a progressive decrease in the volume fraction of smooth muscle elements within the bladder4,5. The end result is either an organ with a thick fibrous wall, low capacity, poor compliance, and little or no contractile function; or, a dilated bladder with a thin fibrous wall, high capacity and little or no contractile function.