Passive detrusor smooth muscle exhibits both viscoelastic softening and strain softening. Strain softening is a loss of stiffness following a stretch to a longer length and is reversible upon muscle activation. Because of this behavior, steady state passive force in detrusor is not constant for a given muscle length and can be adjusted by an intracellular mechanism. Thus, passive detrusor exhibits adjustable passive stiffness. Existing three-component mechanical models for muscle, the Kelvin and Voigt, are insufficient to display this characteristic. The goal of this thesis is to develop a new biomechanical model for passive force in detrusor by adding additional elements to the Kelvin or Voigt models. Eight mechanical characteristics of detrusor are identified from the literature and with three new experiments, and a novel adjustable passive stiffness model for smooth muscle is proposed. Simulations are performed to demonstrate that the model qualitatively exhibits each of the eight tissue characteristics.

Overactive bladder (OAB), involuntary contractions during bladder filling, is a common condition affecting 17% of the adult population worldwide, and in the U.S. ranks ahead of diabetes in a list of the 10 most common chronic disorders (Mullins 2009). Mechanical mechanisms contributing to OAB are not completely understood and because of the unique function and broad volume range of the bladder, there may be mechanical characteristics that distinguish detrusor smooth muscle (DSM) in bladder from other smooth muscles. Recent studies have shown that the length-passive tension curve in DSM exhibits adjustable passive stiffness (APS) characterized by a passive curve that can be shifted along the length axis as a function of strain history and activation history; however, the mechanical mechanisms responsible for APS remain to be determined. Also, whether DSM exhibits a dynamic length-active tension relationship, as has been identified in airway and vascular smooth muscles, has not been investigated. This dissertation focused on both the passive and active length-tension relationships in DSM and the mechanical mechanisms responsible for these relationships. The first objective was to study the impact of APS on the length-total tension relationship and identify the mechanical mechanisms responsible for generating APS. The second objective was to determine whether the length-active tension relationship is adaptive and identify specific mechanical mechanisms contributing to any adaptive behavior. The results showed that a shift in the length-passive tension curve due to APS corresponded with a shift in the length-total tension curve in DSM, and that APS was 27.0±8.4% of active tension at the optimum length for active tension generation. Most importantly, low-grade rhythmic contraction (RC), which can occur spontaneously in rabbit and human bladders, regenerated APS. Results also showed that the length-active tension curve shifted due to stretch to and then activation at long lengths, as well as either multiple KCl-induced maximal contractions or RC. Thus, DSM exhibits length adaptation, and RC may contribute to both APS and length adaptation. Because increased RC has been correlated with OAB, understanding RC, APS and length-adaptation in bladder may enable the identification of specific targets for new treatments for OAB.