Abstract
1. The effect of streptozotocin (STZ)-induced diabetes on cholinergic motor transmission in the rat urinary bladder was investigated by recording contractile activity of detrusor strips in vitro. 2. The Ca(2+)-channel antagonist, nifedipine, was found to be more effective in blocking the noncholinergic motor transmission than P2-purinoceptor desensitization by alpha,beta-methylene ATP. 3. The neurogenic contractile responses to electrical field stimulation in the presence of nifedipine (cholinergic) were larger in the diabetic detrusor than in the non-diabetic controls. The potentiation of the cholinergic transmission was more evident at higher frequencies. 4. Concentration-response curves for acetylcholine were identical in detrusors from diabetic and non-diabetic animals, thus excluding a postsynaptic supersensitivity to acetylcholine being responsible for the potentiation of cholinergic motor transmission. 5. It is concluded that the potentiation of cholinergic motor transmission is due to enhanced release of acetylcholine in diabetic detrusor. Possible reasons for this enhancement are discussed in relation to diabetes.