Presynaptic control of noradrenaline release from sympathetic nerves in human dental pulp.

This study was undertaken to determine whether release of noradrenaline from sympathetic nerves in human dental pulp in vitro was modulated by presynaptic adrenoceptors and by dopamine receptors. Pulp was incubated for 30 min with 3H-noradrenaline (0.6 mumol/l) and then perfused continuously with Krebs solution. Field stimulation of the sympathetic nerves at 5 Hz increased the overflow of 3H into the perfusate three-to fourfold. The stimulation-induced overflow of 3H was abolished by tetrodotoxin (0.1 mumol/l) and under Ca(2+)-free conditions, indicating that the increased 3H was derived from nerves. The stimulation-induced overflow was inhibited by noradrenaline (0.1 and 1.0 mumol/l), the alpha 2-adrenoceptor agonist UK14,304 (0.1 mumol/l), dopamine (1.0 mumol/l) and the dopamine receptor agonist, apomorphine (1.0 mumol/l). When the receptor agonists were noradrenaline or dopamine, desipramine (0.3 or 3.0 mumol/l) was present to prevent their uptake by the sympathetic nerves. Clonidine (1.0 mumol/l; tested at 2 Hz as well as 5 Hz) and the alpha 1-receptor agonist methoxamine (1.0 mumol/l) were without effect. The alpha 2-receptor antagonist/rauwolscine (0.1 mumol/l) prevented the inhibitory effects of noradrenaline and UK14,304, but had little effect on the inhibition produced by dopamine. Inhibition of the stimulation-induced overflow by apomorphine was prevented by the dopamine receptor antagonist haloperidol (0.1 mumol/l). The resting overflow of 3H was unaffected by any of the above agents except dopamine, which caused a small increase. It is concluded that the sympathetic nerves in human dental pulp possess inhibitory presynaptic alpha 2-adrenoceptors and dopamine receptors.(ABSTRACT TRUNCATED AT 250 WORDS)