Functional, morphological and molecular characterization of bladder dysfunction in streptozotocin‐induced diabetic mice: evidence of a role for L‐type voltage‐operated Ca²⁺ channels

Abstract

Diabetic mice exhibit features of urinary bladder dysfunction, as characterized by overactive DSM and decreased voiding efficiency. Functional and molecular data suggest that overactive DSM in diabetes is the result of enhanced extracellular Ca(2+) influx through L-VOCC.