Previous morphological and physiological studies have suggested that the adrenergic innervation of the dorsal motor nucleus of the vagus nerve (dmnX) is involved in direct synaptic inhibition of parasympathetic preganglionic neurones of the vagus that control secretion of pancreatic insulin. We investigated the effects of bilateral 6-hydroxydopamine (6-OHDA) lesions of adrenergic innervation of the dmnX on pancreatic insulin secretion and glycaemia in normal and vagotomized rats. After two weeks the 6-OHDA lesions produced a marked increase in circulating insulin levels, but no change in glycaemia. Hyperinsulinaemia after adrenergic denervation of the dmnX was more pronounced when a glucose bolus was injected intraarterially. Bilateral subdiaphragmatic vagotomy reversed the observed hyperinsulinaemia. This targeted pharmacological lesion of the adrenergic innervation of dmnX thus causes hypersecretion by pancreatic B cells, an effect which requires an intact vagus nerve.
Data concerning the effect of NO on the function and structure of the heart are controversiaL We have studied two main questions: (i) Does the heart muscle reflect the hypertension induced by long-term inhibition of NO synthase? (ii) Since the arginine-NO pathway is also operative in the autonomic nervous system, the second goal was to ascertain the possible changes of the adrenergic nervous system in the heart after long-term NO synthase inhibition. Wistar rats were administered L-NAME in drinking water (50 mg/kg bw/day) for 8 weeks. Systolic blood pressure and heart rate were monitored weekly. The heart/body weight ratio were determined at the end of experiment The adrenergic nerve terminals visualized by histochemistry were counted according to Haug’s point counting method. Blood pressure increased significantly in L-NAME-treated rats. No changes were found in the heart rate. Heart/body weight ratio increased markedly. Surprisingly, the density of adrenergic nerve terminals did not alter accordingly. The density of adrenergic nerve terminals in the left ventricle and septum decreased but no significant changes were found in the left atrium and the right ventricle. Hypertension due to NO deficiency induced cardiac hypertrophy that was characterized by a decline in the density of adrenergic innervation of the overloaded left ventricle and septum.