Non-adrenergic, non-cholinergic influences on parotid acinar degranulation in response to stimulation of the parasympathetic innervation in the anaesthetized rat.

Abstract

In pentobarbitione-anaesthetized rats the parasympathetic auriculotemporal nerve of the parotid gland was continuously stimulated at supramaximal voltage and at maximal frequency (40 Hz) for salivary secretion. The animals were pretreated with phentolamine and propranolol (2 mg kg-1 i.p. of each) and, in some groups, additionally with atropine (2 mg kg-1 i.p.). Morphometric assessment at the light microscopic level (x 100) showed that the numerical density of parotid acinar secretory granules (per 100 microns2 acinar epithelial cytoplasm) was reduced by 30 and 39% after 40 and 80 min, respectively, of stimulation in non-atropinized animals and by 30 and 27% in atropinized animals. The numerical density of acinar granules was not influenced by pretreatment with the protein synthesis inhibitor cycloheximide. The results suggest that most of the parasympathetic nerve-induced degranulation in the absence of muscarinic receptor blockade can be attributed to the action of non-adrenergic, non-cholinergic mechanisms.