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A parotid acinar degranulation of approximately 60 and 40% was observed in cats under pentobarbitone anaesthesia after a 90-min period of continuous stimulation of the parasympathetic auriculo-temporal nerve at 10 Hz in the absence and presence of atropine, respectively. Atropine completely abolished the large fluid response of the gland to the nerve stimulation. In the non-atropinized cats, bethanechol, infused into the carotid artery at a dose rate evoking a salivary flow similar to that in response to parasympathetic nerve stimulation, caused an acinar degranulation of approximately 25% and acinar vacuolation. Vasoactive intestinal peptide (VIP; 0.5 microgram kg-1 min-1 also infused into the carotid artery for 90 min) caused an acinar degranulation of the same magnitude as the parasympathomimetic drug but the peptide did not give rise to any fluid secretion or vacuole formation. The experiments were performed in the presence of alpha- and beta-adrenoceptor blockers. Thus, in parotid glands of the cat, producing no overt secretion of fluid, non-adrenergic, non-cholinergic (NANC) mechanisms may be at work causing exocytosis of the acinar granules. These mechanisms are also likely to contribute to the secretion of granules in response to parasympathetic nerve activity in the absence of blockade of the classical autonomic receptors.

SUMMARYIn 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-' 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 l um2 acinar epithelial cytoplasm) was reduced by 30 and 390% 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.

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