Das. Parker et al., PRESYNAPTIC CONTROL OF NORADRENALINE RELEASE FROM SYMPATHETIC-NERVES IN HUMAN DENTAL-PULP, Archives of oral biology, 39(1), 1994, pp. 35-41
This study was undertaken to determine whether release of noradrenalin
e from sympathetic nerves in human dental pulp in vitro was modulated
by presynaptic adrenoceptors and by dopamine receptors. Pulp was incub
ated for 30 min with H-3-noradrenaline (0.6 mu mol/l) and then perfuse
d continuously with Krebs solution. Field stimulation of the sympathet
ic nerves at 5 Hz increased the overflow of H-3 into the perfusate thr
ee-to fourfold. The stimulation-induced overflow of H-3 was abolished
by tetrodotoxin (0.1 mu mol/l) and under Ca2+-free conditions, indicat
ing that the increased H-3 was derived from nerves. The stimulation-in
duced overflow was inhibited by noradrenaline (0.1 and 1.0 mu mol/l),
the alpha(2)-adrenoceptor agonist UK14,304 (0.1 mu mol/l), dopamine (1
.0 mu mol/l) and the dopamine receptor agonist, apomorphine (1.0 mu mo
l/l). When the receptor agonists were noradrenaline or dopamine, desip
ramine (0.3 or 3.0 mu mol/l) was present to prevent their uptake by th
e sympathetic nerves. Clonidine (1.0 mu mol/l; tested at 2 Hz as well
as 5 Hz) and the alpha(1)-receptor agonist methoxamine (1.0 mu mol/l)
were without effect. The alpha(2)-receptor antagonist/rauwolscine (0.1
mu mol/l) prevented the inhibitory effects of noradrenaline and UK14,
304, but had little effect on the inhibition produced by dopamine. Inh
ibition of the stimulation-induced overflow by apomorphine was prevent
ed by the dopamine receptor antagonist haloperidol(0.1 mu mol/l). The
resting overflow of H-3 was unaffected by any of the above agents exce
pt dopamine, which caused a small increase. It is concluded that the s
ympathetic nerves in human dental pulp possess inhibitory presynaptic
alpha(2)-adrenoceptors and dopamine receptors. As the stimulation-indu
ced overflow was increased by rauwolscine, but not by haloperidol, it
is suggested that the alpha(2)-adrenoceptor plays a physiological role
in modulating sympathetic transmission, but this may not apply to the
dopamine receptor.