Purpose PACAP and receptors are expressed in micturition pathways. Studies show that PACAP has a role in detrusor smooth muscle contraction to facilitate adenosine triphosphate release from urothelium and PACAP antagonism decreases cyclophosphamide induced bladder hyperreflexia. Materials and Methods PACAP contributions to micturition and somatic sensation were studied in PACAP knockout (PACAP −/−), litter mate heterozygote (PACAP +/−) and WT mice by conscious cystometry with continuous intravesical saline or acetic acid (0.5%) instillation, urination patterns, somatic sensitivity testing of hind paw and pelvic regions with calibrated von Frey filaments, and morphological bladder assessments. Results PACAP −/− mice had an increased bladder mass with fewer but larger urine spots. In PACAP −/− mice the lamina propria and detrusor smooth muscle were significantly thicker but the urothelium was unchanged. PACAP −/− mice had increased bladder capacity, voided volume and intercontraction interval with significantly increased detrusor contraction duration and large residual volume. WT mice responded to acetic acid (0.5%) with a decrease in voided volume and intercontraction interval but PACAP +/− and PACAP −/− mice did not respond. PACAP −/− mice were less responsive to somatic stimulation. PACAP +/− mice also had bladder dysfunction, and somatic and visceral sensory abnormalities but to a lesser degree. Conclusions PACAP gene disruption contributes to changes in bladder morphology and function, and somatic and visceral hypoalgesia.