Modulation by presynaptic β-adrenoceptors of noradrenaline release from sympathetic nerves in human dental pulp

This study was undertaken to test for the presence of presynaptic β-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 μmol/l) and subsequently superfused with Krebs solution. Sympathetic nerves were stimulated at 5 Hz for 100 sec. The non-specific β-adrenoceptor agonist isoprenaline (1.0 μmol/l), and the selective β2-agonist salbutamol (10 μmol/l) facilitated the release of [3H]-noradrenaline; isoprenaline, but not salbutamol, also facilitated this release in the presence of desipramine (DMI, 0.3 μmol/l), corticosterone (10 μmol/l) and rauwolscine (0.1 μmol/l). BRL 37344 (1.0 μmol/l), a β3-agonist, had no effect on [3H]-noradrenaline release. The facilitatory effects of isoprenaline and salbutamol were inhibited by the non-specific β-antagonist propranolol (1.0 μmol/l), while that of salbutamol was inhibited in the presence of ICI-188,551 (1.0 μmol/l), a selective β2-antagonist, as well. The β1-antagonist atenolol (1.0 μmol/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 β-adrenoceptors on sympathetic nerves in human dental pulp. It is suggested that they are of the β2-subtype, although a greater range of agonists and antagonists needs to be used to clarify the nature of the β-adrenoceptors.