Nitric oxide (NO) is a likely parasympathetic nonadrenergic, noncholinergic transmitter in parotid glands, since parasympathetic nerves contain NO-synthase. Parasympathetic stimulation (30 min, atropine + phentolamine + propranolol) increased the protein synthesis ([³H] leucine uptake) by 142% (10 Hz) and 200% (40 Hz). Surprisingly, neither the neuronal type NO-synthase inhibitor N-PLA, nor the unspecific inhibitor L-NAME reduced the response. Moreover, the parasympathetic nonadrenergic, noncholinergic (40 Hz, 30 min)-evoked increase (65%) in mitotic activity ([³H] thymidine uptake) was unaffected by the NO-synthase inhibitors. Sympathetic nerves lack NO-synthase, yet inhibition of NO-generation reduced the β-adrenoceptor mediated response to sympathetic stimulation. Whereas the protein synthesis increased by 192% to stimulation (50 Hz, 1s every tenth s for 30 min) under just α-adrenoceptor blockade, the response was more than halved in the presence of N-PLA to 86%) or L-NAME to 91%). Furthermore, the β-adrenoceptor mediated increase in mitotic activity 122%) to sympathetic stimulation 20 Hz, 4 min every fifth min for 30 min), under α-adrenoceptor blockade, was reduced to 49% N-PLA) and 47% (L-NAME). Pentagastrin (20 µg/kg, I. V. infused for one h) increased the protein synthesis by 17%. N-PLA prevented this increase but did not affect the basal protein, while cholecystokinin receptor blockers reduced both the basal protein synthesis (by 20%), and the pentagastrin-induced increase. Thus, implying that strong rather than weak stimuli of the cholecystokinin receptors activate neuronal type NO-synthase. Despite being of the neuronal type, the NO-synthase generating NO in response to stimulation of β-adrenoceptors or cholecystokinin receptors was probably of parenchymal origin.