Evidence for presynaptic cholinergic receptors in sympathetic nerves in human dental pulp.
The purpose of this study was to determine whether presynaptic cholinergic receptors are present in sympathetic nerves in human dental pulp. Pulp was incubated with [3H]noradrenaline (0.6 mumol/l) for 30 min and then superfused with Krebs' solution at 1.0 ml/min. Electrical stimulation (100 sec, 5 Hz) increased the overflow of [3H]noradrenaline into the superfusate. Carbachol (10 and 100 mumol/l), an agonist of muscarinic receptors, decreased the stimulation-induced (SI) overflow of 3H, an effect blocked by atropine but not hexamethonium. Carbachol, atropine and hexamethonium had no effect on the resting overflow. Nicotine (10 mumol/l) increased the resting overflow and inhibited the SI overflow, although the inhibition was variable. Cytisine, another agonist of nicotinic receptors, also increased the resting overflow, but did not affect the SI overflow. To ascertain whether the actions of nicotine and electrical stimulation were influenced by the release of nitric oxide (NO), the effects of an NO donor and two NO-synthase inhibitors were examined. With the exception of one of the NO-synthase inhibitors (L-NAME), the agents were without effect on the overflow of 3H in the absence or presence of nicotine. It was concluded that sympathetic nerves in human dental pulp possess (a) presynaptic muscarinic receptors that inhibit the SI release of noradrenaline, and (b) nicotinic receptors that evoke the release of noradrenaline and that inhibit the SI release of the transmitter. The results do not point to a significant role for NO in the effects of stimulation or nicotine on the overflow of 3H.
Parker
D A
DA
Department of Dentistry, University of Adelaide, South Australia.
Marino
V
V
Zisimopoulos
S
S
de la Lande
I S
IS
D000293:Adolescent; D000328:Adult; D000470:Alkaloids / Q000494:pharmacology; D001285:Atropine / Q000494:pharmacology; D001392:Azocines; D002217:Carbachol / Q000494:pharmacology; D003782:Dental Pulp / Q000294:innervation*; D004558:Electric Stimulation; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D018738:Hexamethonium / Q000494:pharmacology; D006801:Humans; D007552:Isotonic Solutions; D008297:Male; D018721:Muscarinic Agonists / Q000494:pharmacology; D018727:Muscarinic Antagonists / Q000494:pharmacology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009538:Nicotine / Q000494:pharmacology; D018722:Nicotinic Agonists / Q000494:pharmacology; D018733:Nicotinic Antagonists / Q000494:pharmacology; D009569:Nitric Oxide / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D009638:Norepinephrine / Q000494:pharmacology; D011807:Quinolizines; D019275:Radiopharmaceuticals; D011976:Receptors, Muscarinic / Q000187:drug effects / Q000648:ultrastructure*; D011978:Receptors, Nicotinic / Q000187:drug effects / Q000648:ultrastructure; D017661:Receptors, Presynaptic / Q000037:antagonists & inhibitors / Q000187:drug effects / Q000648:ultrastructure*; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000648:ultrastructure*; D013566:Sympathomimetics / Q000494:pharmacology; D014316:Tritium; D000093843:Quinolizidine Alkaloids
D000470:Alkaloids; D001285:Atropine; D001392:Azocines; D002217:Carbachol; D004791:Enzyme Inhibitors; D018738:Hexamethonium; D007552:Isotonic Solutions; D018721:Muscarinic Agonists; D018727:Muscarinic Antagonists; D019331:NG-Nitroarginine Methyl Ester; D009538:Nicotine; D018722:Nicotinic Agonists; D018733:Nicotinic Antagonists; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D009638:Norepinephrine; D011807:Quinolizines; D019275:Radiopharmaceuticals; D011976:Receptors, Muscarinic; D011978:Receptors, Nicotinic; D017661:Receptors, Presynaptic; D013566:Sympathomimetics; D014316:Tritium; C051865:Krebs-Ringer solution; C004712:cytisine; D000093843:Quinolizidine Alkaloids