DEPLETION OF SECRETORY GRANULES FROM THE FELINE PAROTID-GLAND - ACTION OF NANC TRANSMITTERS PER SE

A parotid acinar degranulation of approximately 60 and 40% was observe d in cats under pentobarbitone anaesthesia after a 90-min period of co ntinuous 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 ner ve 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 acina r degranulation of approximately 25% and acinar vacuolation. Vasoactiv e intestinal peptide (VIP;0.5 mu g kg(-1) min(-1) also infused into th e carotid artery for 90 min) caused an acinar degranulation of the sam e magnitude as the parasympathomimetic drug but the peptide did not gi ve rise to any fluid secretion or vacuole formation. The experiments w ere 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 wor k causing exocytosis of the acinar granules. These mechanisms are also likely to contribute to the secretion of granules in response to para sympathetic nerve activity in the absence of blockade of the classical autonomic receptors.