Physiological and pathophysiological implications of micromotion activity in urinary bladder function.

Abstract

'Micromotions' is a term signifying the presence of localized microcontractions and microelongations, alongside non-motile areas. The motile areas tend to shift over the bladder surface with time, and the intravesical pressure reflects moment-by-moment summation of the interplay between net contractile force generated by micromotions and general bladder tone. Functionally, the bladder structure may comprise modules with variable linkage, which supports presence of localized micromotions (no functional linkage between modules), propagating contractions (where emergence of linkage allows sequential activation) and the shifting of micromotions over time. Detrusor muscle, interstitial cells and intramural innervation have properties potentially relevant for initiating, coordinating and modulating micromotions. Conceptually, such activity could facilitate the generation of afferent activity (filling state reporting) in the absence of intravesical pressure change and the ability to transition to voiding at any bladder volume. This autonomous activity is an intrinsic property, seen in various experimental contexts including the clinical setting of human (female) overactive bladder. 'Disinhibited autonomy' may explain the obvious micromotions in isolated bladders and perhaps contribute clinically in neurological disease causing detrusor overactivity. Furthermore, any process that could increase the initiation or propagation of microcontractions might be anticipated to have a functional effect, increasing the likelihood of urinary urgency and detrusor overactivity respectively. Thus, models of bladder outlet obstruction, neurological trauma and ageing provide a useful framework for detecting cellular changes in smooth muscle, interstitial cells and innervation, and the consequent effects on micromotions.