Modeling the influence of acute changes in bladder elasticity on pressure and wall tension during filling.

Tension-sensitive nerves in the bladder wall are responsible for providing bladder sensation. Bladder wall tension, and therefore nerve output, is a function of bladder pressure, volume, geometry and material properties. The elastic modulus of the bladder is acutely adjustable, and this material property is responsible for adjustable preload tension exhibited in human and rabbit detrusor muscle strips and dynamic elasticity revealed during comparative-fill urodynamics in humans. A finite deformation model of the bladder was previously used to predict filling pressure and wall tension using uniaxial tension test data and the results showed that wall tension can increase significantly during filling with relatively little pressure change. In the present study, published uniaxial rabbit detrusor data were used to quantify regulated changes in the elastic modulus, and the finite deformation model was expanded to illustrate the potential effects of elasticity changes on pressure and wall tension during filling. The model demonstrates a shift between relatively flat pressure-volume filling curves, which is consistent with a recent human urodynamics study, and also predicts that dynamic elasticity would produce significant changes in wall tension during filling. The model results support the conclusion that acute regulation of bladder elasticity could contribute to significant changes in wall tension for a given volume that could lead to urgency, and that a single urodynamic fill may be insufficient to characterize bladder biomechanics. The model illustrates the potential value of quantifying wall tension in addition to pressure during urodynamics.

Evidence for a common mechanism for spontaneous rhythmic contraction and myogenic contraction induced by quick stretch in detrusor smooth muscle.

Detrusor smooth muscle exhibits myogenic contraction in response to a quick stretch (QS) as well as spontaneous rhythmic contraction (SRC); however, whether the same population of actomyosin crossbridges with a common regulatory mechanism is responsible for these two types of contraction has not been determined. Detrusor strips from New Zealand white rabbit bladders were allowed to develop SRC at a reference muscle length (L ref), or rhythmic contraction (RC) was induced with tetraethylammonium (TEA). Multiple 10-msec stretches of 15% L ref were then imposed at L ref randomly during the rhythm cycle, and the nadir-to-peak (NTP) tension amplitude of the resulting myogenic contraction was measured. The amplitude and period of the rhythm cycle were measured prior to each QS. NTP was larger when a QS was imposed during a portion the cycle when tension was smaller (n = 3 each SRC and TEA-induced RC). These data suggest that when the rhythmic mechanism was mostly inactive and tension was near a minimum, a larger portion of a shared population of crossbridges was available to produce a myogenic response to a QS. Rho kinase, cyclooxygenase-1, and cyclooxygenase-2 inhibitors (H-1152, SC-560, and NS-398) affected SRC amplitude and NTP amplitude following a QS to the same degree (n = 3 each drug), providing additional evidence to support the hypothesis that a common mechanism is responsible for SRC and myogenic contraction due to QS. If a common mechanism exists, then QS is a potential mechanical probe to study SRC regulation and its alteration in overactive bladder.