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.

Report and Research Agenda of the American Geriatrics Society and National Institute on Aging Bedside‐to‐Bench Conference on Urinary Incontinence in Older Adults: A Translational Research Agenda for a Complex Geriatric Syndrome

“…A significant problem with this etiological model is the lack of clear interdependence between symptoms (OAB, UAB) and function (DO, DU) demonstrated during urodynamic assessment . An emerging therapeutic model, which may be particularly relevant for older adults, addresses abnormal generation of bladder volume sensory afferent activity due to abnormal focal tensions in the bladder wall or activation of atypical sensory pathways as an etiological pathway for urinary storage symptoms such as OAB and UAB …”

Corticotrophin-Releasing Hormone neurons of Barrington’s nucleus: Probabilistic, spinally-gated control of bladder pressure and micturition

“…There has been considerable debate about the origin of NVCs with respect to whether they are intrinsically generated by the bladder and their functional significance although there is a suggestion that they provide a means to infer the degree of bladder filling 56 . An increase in their frequency and amplitude has been linked to diseases of the LUT 57 and also with loss of descending control from the brainstem 6 which could conceivably be related to the loss of CRH-mediated spinal inhibition. There is also evidence of their peripheral generation by the bladder early in development which becomes less coordinated in adult bladder 58 .…”

In vitro culture of rat hair follicle stem cells on rabbit bladder acellular matrix

“…Usually, autologous non-urologic tissue or synthetic polymeric materials were used to repair or replace the bladder defect. However, since these materials cannot fully replace the function of the original tissues and organs, they can result in several adverse effects (Sumino and Mimata 2013; Xie et al 2015; Kulikov et al 2015; Alberti 2013; Vahabi and Drake 2015). Moreover, the limited resource of autological non-urologic tissues represents an additional obstacle.…”