Adrenergic, but not cholinergic or purinergic, responses are potentiated in the cecum of diabetic rats.

Electrophysiologic properties of smooth muscle strips from the circular muscle of the cecum were compared in streptozocin-treated diabetic (8 wk) and untreated control rats using the sucrose-gap technique. Changes in membrane potential elicited by field stimulation (0.03-32 Hz) and by exogenously applied adenosine triphosphate (10-1000 microM) and noradrenaline (0.03-10 microM) were measured. Nonadrenergic, noncholinergic inhibitory junction potentials were the predominant response to field stimulation. However, in some preparations from both diabetic and control tissues, the inhibitory junction potential was preceded by a small nonadrenergic, noncholinergic excitatory junction potential. In nonatropinized preparations, a cholinergic excitatory junction potential was occasionally elicited; there was no difference between these cholinergic responses in diabetic and control tissues. The inhibitory junction potentials and the hyperpolarization in response to adenosine triphosphate were similar in diabetic and control tissues, although the rate of hyperpolarization of the single inhibitory junction potential was slower in the diabetic tissues. In contrast, exogenous application of noradrenaline revealed significantly greater hyperpolarizing responses in diabetic compared with control tissues. This increase in potency appeared to be due, in part, to an increased sensitivity of alpha-adrenoceptors on smooth muscle. There was no evidence for beta-adrenoceptor activation by noradrenaline. Prejunctional inhibition of the nonadrenergic, noncholinergic neuromuscular transmission by noradrenaline was not affected by streptozocin-induced diabetes. The induced changes in adrenoceptor activity were selective for the postjunctional alpha-adrenoceptors.