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 Ca2+-channel antagonist, nifedipine, was found to be more effective in blocking the non-cholinergic motor transmission than P2-purinoceptor desensitization by α,β-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.