Impairment of urinary bladder mechanical properties in rat model of type 2 diabetes.

Aims: The urinary bladder is a mechanosensitive organ that accumulates, stores, and expels considerable amounts of fluid. While the neuronal bladder control via the CNS is well defined, the data on the mechanisms of local mechanical sensitivity of the bladder wall are either insufficient or contradictory. Here we compared the mechanical properties of bladder wall of normal rats and rats with modeled type 2 diabetes (T2D).

Methods: T2D was modeled in 3-month-old Wistar male rats by combined administration of nicotinamide (230 mg/kg) and streptozotocin (65 mg/kg). Cystometry of isolated, denervated whole bladders and stress-strain tensiometry on detrusor smooth muscle (DSM) strips were used to assess the mechanical properties of bladder wall tissues from control and diabetic animals on 10th week after induction.

Results: The pressure-volume cystometrograms of both control and T2D bladders featured a quasi plateau between ascending sections. T2D cystometrograms revealed markedly elevated intravesicular pressure (~100% at 1 ml) and a shortened plateau, consistent with decreased bladder wall elasticity and reduced structural bladder capacity versus control. Experiments on urothelium-intact and urothelium-devoid DSM strips have shown that the decrease of bladder walls elasticity in T2D can be explained by the switch of stretched urothelium from inducing DSM relaxation to inducing DSM contraction due to a change in the prevalent release of contractile versus relaxing urothelial factor(s).

Conclusions: The decreased elasticity of the bladder walls in T2D results from alterations in urothelium-dependent mechanosensory mechanisms. Elevated intravesical pressure in T2D may contribute to urge incontinence and/or symptoms of upper urinary tract damage.