Strips of rabbit detrusor smooth muscle (DSM) exhibit adjustable passive stiffness characterized by strain softening - a loss of stiffness upon stretch to a new length distinct from viscoelastic behavior. At the molecular level, strain softening appears to be caused by crosslink breakage, and is essentially irreversible when DSM is maintained under passive conditions (i.e., when crossbridges are not cycling to produce active force). However, upon DSM activation, strain softening is reversible and likely due to crosslink reformation. Thus, DSM displays adjustable passive stiffness that is dependent on the history of both muscle strain and activation. The present study provides empirical data showing that in DSM, 1) passive isometric force relaxation includes a very slow component requiring hours to approach steady state, 2) the level of passive force maintained at steady state is less if the tissue has previously been strain softened, and 3) tissues subjected to a quick-release protocol exhibit a biphasic response consisting of passive force redevelopment followed by force relaxation. To explain these and previously identified characteristics, a mechanical model for adjustable passive stiffness is proposed based on the addition of a novel crosslinking element to a hybrid Kelvin/Voigt viscoelastic model.