title: Modulation by presynaptic beta-adrenoceptors of noradrenaline release from sympathetic nerves in human dental pulp.
abstract: This study was undertaken to test for the presence of presynaptic beta-adrenoceptors on sympathetic nerves in human dental pulp and, if present, to investigate the subtype. Pulp was excised from freshly extracted teeth, incubated with [3H]-noradrenaline (0.6 micromol/l) and subsequently superfused with Krebs solution. Sympathetic nerves were stimulated at 5 Hz for 100 sec. The non-specific beta-adrenoceptor agonist isoprenaline (1.0 micromol/l), and the selective beta2-agonist salbutamol (10 micromol/l) facilitated the release of [3H]-noradrenaline; isoprenaline, but not salbutamol, also facilitated this release in the presence of desipramine (DMI, 0.3 micromol/l), corticosterone (10 micromol/l) and rauwolscine (0.1 micromol/l). BRL 37344 (1.0 micromol/l), a beta3-agonist, had no effect on [3H]-noradrenaline release. The facilitatory effects of isoprenaline and salbutamol were inhibited by the non-specific beta-antagonist propranolol (1.0 micromol/l), while that of salbutamol was inhibited in the presence of ICI-188,551 (1.0 micromol/l), a selective beta2-antagonist, as well. The beta1-antagonist atenolol (1.0 micromol/l) potentiated the facilitatory effects of isoprenaline in the presence of DMI and corticosterone. Neither propranolol nor ICI-188,551 alone affected the release of [3H]-noradrenaline. These results establish the presence of presynaptic beta-adrenoceptors on sympathetic nerves in human dental pulp. It is suggested that they are of the beta2-subtype, although a greater range of agonists and antagonists needs to be used to clarify the nature of the the beta-adrenoceptors.
authors.affiliation: Department of Dentistry, The University of Adelaide, South Australia.
authors.forename: D A
authors.initials: DA
authors.lastname: Parker
authors.forename: V
authors.initials: V
authors.lastname: Marino
authors.forename: P M
authors.initials: PM
authors.lastname: Ivar
authors.forename: I S
authors.initials: IS
authors.lastname: de la Lande
mesh_terms: D000293:Adolescent; D018759:Adrenergic Uptake Inhibitors / Q000494:pharmacology; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000328:Adult; D000420:Albuterol / Q000494:pharmacology; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D003345:Corticosterone / Q000494:pharmacology; D003782:Dental Pulp / Q000294:innervation*; D003891:Desipramine / Q000494:pharmacology; D004558:Electric Stimulation; D004983:Ethanolamines / Q000494:pharmacology; D005260:Female; D006801:Humans; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D009638:Norepinephrine / Q000378:metabolism*; D011433:Propranolol / Q000494:pharmacology; D019275:Radiopharmaceuticals; D011943:Receptors, Adrenergic, beta / Q000187:drug effects / Q000502:physiology*; D017661:Receptors, Presynaptic / Q000187:drug effects / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology; D013565:Sympatholytics / Q000494:pharmacology; D013566:Sympathomimetics / Q000378:metabolism*; D014316:Tritium; D015016:Yohimbine / Q000494:pharmacology
chemical_list: D018759:Adrenergic Uptake Inhibitors; D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D000893:Anti-Inflammatory Agents; D004983:Ethanolamines; D019275:Radiopharmaceuticals; D011943:Receptors, Adrenergic, beta; D017661:Receptors, Presynaptic; D013565:Sympatholytics; D013566:Sympathomimetics; D014316:Tritium; D015016:Yohimbine; C057368:BRL 37344; D011433:Propranolol; D007545:Isoproterenol; D000420:Albuterol; D003891:Desipramine; D003345:Corticosterone; D009638:Norepinephrine