Murine in vitro whole bladder physiology.

Abstract

The function of the bladder is twofold: 1) to store urine at low pressure, and 2) under control of the nervous system, to generate a contractile force coordinated with a lowered urethral resistance that allows for emptying.20 Clinically, this system is most commonly affected by bladder outlet obstruction, and the response of the detrusor is remarkable in its variability. Experimentally, most investigators agree that after outlet obstruction, there is an increase in bladder mass seen irrespective of the model used. Within most experimental models of partial obstruction (as with humans), there exists a degree of variability in terms of detrusor response. Some bladders enter a state of compensation and are able to sustain elevated voiding pressures and empty satisfactorily. Others enter a state of decompensation and lose their ability to empty effectively.15 The molecular mechanisms for such decompensations are under current investigation, and may involve alterations in cytosolic calcium handling,19,21 disruptions in mitochondrial function,4 and changes in the expression of contractile filaments.1 In the late stages, as the bladder slides into the decompensated state, major depositions of extracellular matrix are seen in a variety of species.3,9,11