Diabetes was induced with streptozocin in male Wistar rats. After 4–6 mo, parotid salivary flow was induced by stimulating bipolar electrodes (3–5 V for 2 ms) on either the auriculotemporal nerve (5 Hz) or the cervical sympathetic trunk (10 Hz). During parasympathetic stimulation, flow rates were 443 ± 287 μl/30 min in diabetic animals compared to 657 ± 134 μl/30 min in controls (P < .01). Although parotid flow rates during parasympathetic stimulation were well maintained in controls, they decreased rapidly in most diabetic rats. Parotid secretory response to sympathetic stimulation was also reduced in diabetic compared with control animals (40 ± 16 μl/30 min and 82 ± 50 μl/30 min, respectively, P < .01). In contrast to results obtained with direct neural stimulation, no differences in threshold dose or total saliva were observed when cholinergic (methacholine) and peptidergic (physalaemin) agonists were administered intravenously. Response threshold for an adrenergic agonist (epinephrine) was significantly increased in diabetes. Electron microscopy showed axoplasmic abnormalities in nonmyelinated axons in diabetic glands but not in control glands. Although most nerve profiles appeared normal, neuroaxonal abnormalities were found in every diabetic animal. The ultrastructural findings and the similar responses to methacholine and physalaemin suggest that autonomie neuropathy may be a factor in the abnormal response of the parotid gland to parasympathetic nerve stimulation.

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