Abnormalities of rat bladder contractility in streptozotocin-induced diabetes mellitus.

Diabetic cystopathy is a common complication of diabetes mellitus, but little is known of the mechanisms responsible for the bladder dysfunction. Therefore, the effect of streptozotocin-induced diabetes on urinary bladder function was investigated. Bladders from 2-month diabetic rats were significantly larger than those from age-matched controls. Protein concentrations in bladder body and base were similar in diabetic and control rats. However, due to the greater bladder body weight in diabetic animals, total protein content of bladder bodies from diabetic rats was significantly greater than those from controls. Contractile responses of strips obtained from bladder body and base to stimulatory agents and nerve stimulation were altered by diabetes. In bladder bodies from diabetic rats, the maximal contractile responses to nerve stimulation, acetylcholine and KCl were reduced compared to controls. In addition there was a decreased sensitivity to acetylcholine and KCl in the diabetics. In contrast, with strips from bladder base there was a decrease in sensitivity to nerve stimulation in the diabetic rats, but no change in sensitivity to norepinephrine, acetylcholine, ATP or KCl. The maximal contraction by bladder base in response to norepinephrine was decreased in diabetic rats, but there was no change in maximal contraction by bladder base in response to norepinephrine was decreased in diabetic rats, but there was no change in maximal response to nerve stimulation, acetylcholine, ATP or KCl. These results indicate that a relatively nonspecific decrease in the responsiveness of bladder body is caused by diabetes, but agonist-specific changes are produced in bladder base.(ABSTRACT TRUNCATED AT 250 WORDS)