Evidence for presynaptic cholinergic receptors in sympathetic nerves in human dental pulp

Autor: D. A. S. Parker, I. S. de la Lande, S. Zisimopoulos, Victor Marino
Rok vydání: 1998
Předmět:
Atropine
Male
Sympathetic Nervous System
Stimulation
Nicotinic Antagonists
Receptors
Nicotinic
Receptors
Presynaptic
Nicotine
Norepinephrine
chemistry.chemical_compound
Muscarinic acetylcholine receptor
Nicotinic Agonists
Enzyme Inhibitors
Sympathomimetics
musculoskeletal
neural
and ocular physiology
General Medicine
musculoskeletal system
Azocines
Receptors
Muscarinic
NG-Nitroarginine Methyl Ester
cardiovascular system
Female
Hexamethonium
Quinolizines
medicine.drug
Adult
Agonist
medicine.medical_specialty
Carbachol
Adolescent
medicine.drug_class
Muscarinic Antagonists
Muscarinic Agonists
Nitric Oxide
Tritium
Cytisine
Alkaloids
Internal medicine
medicine
Humans
General Dentistry
Dental Pulp
Cell Biology
Electric Stimulation
Endocrinology
nervous system
Otorhinolaryngology
chemistry
Cholinergic
Isotonic Solutions
Nitric Oxide Synthase
Radiopharmaceuticals
Zdroj: Archives of Oral Biology. 43:197-204
ISSN: 0003-9969
DOI: 10.1016/s0003-9969(98)00006-5
Popis: 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 [ 3 H]noradrenaline (0.6 μmol/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 [ 3 H]noradrenaline into the superfusate. Carbachol (10 and 100 μmol/l), an agonist of muscarinic receptors, decreased the stimulation-induced (SI) overflow of 3 H, an effect blocked by atropine but not hexamethonium. Carbachol, atropine and hexamethonium had no effect on the resting overflow. Nicotine (10 μmol/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 3 H 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 3 H.
Databáze: OpenAIRE
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