EVIDENCE FOR PRESYNAPTIC CHOLINERGIC RECEPTORS IN SYMPATHETIC-NERVES IN HUMAN DENTAL-PULP

The purpose of this study was to determine whether presynaptic choline rgic receptors are present in sympathetic nerves in human dental pulp. Pulp was incubated with [H-3]noradrenaline (0.6 mu mol/l) for 30 min and then superfused with Krebs' solution at 1.0 ml/min. Electrical sti mulation (100 sec: 5 Hz) increased the overflow of [3H]noradrenaline i nto the superfusate. Carbachol (10 and 100 mu mol/l), an agonist of mu scarinic receptors, decreased the stimulation-induced (SI) overflow of H-3, an effect blocked by atropine but not hexamethonium. Carbachol, atropine and hexamethonium had no effect on the resting overflow. Nico tine (10 mu mol/l) increased the resting overt-low and inhibited the S I overflow, although the inhibition was variable. Cytisine, another ag onist of nicotinic receptors. also increased the resting overflow, but did not affect the SI overflow. To ascertain whether the actions of n icotine and electrical stimulation were influenced by the release of n itric oxide (NO), the effects of an NO donor and two NO-synthase inhib itors were examined. With the exception of one of the NO-synthase inhi bitors (L-NAME), the agents were without effect on the overflow of H-3 in the absence or presence of nicotine. It was concluded that sympath etic nerves in human dental pulp possess (a) presynaptic muscarinic re ceptors that inhibit the SI release of noradrenaline, and (b) nicotini c receptors that evoke the release of noradrenaline and that inhibit t he SI release of the transmitter. The results do not point to a signif icant role for NO in the effects of stimulation or nicotine on the ove rflow of H-3. (C) 1998 Elsevier Science Ltd. All rights reserved.