Tyramine
is an endogenous compound which exists in the brain as a trace amine (Durden
and Davis, 1993), but it is
also an exogenous compound which is found in foods such as cheese and wine. Although the level is very low,
evidence obtained from animal studies has indicated that this trace amine has a very rapid
turnover rate. Its presence in a brain synaptosomal fraction suggests a possible involvement in
the process of neurotransmission (Philips et al., 1978).
There
is a general agreement that the hypertensive action of the indirectly acting sympathomimetic tyramine is due to the
release of norepinephrine from peripheral noradrenergic nerves. However, the mechanism of action of tyramine
in brain regions that are involved
in cardiovascular regulation is largely unknown. Tyramine microinjected into
the rostral ventrolateral
medulla (RVL, C1 area) elicits a dose-dependent decrease in arterial pressure, heart rate and sympathetic renal
nerve activity and this effect was blocked by previous microinjection desmethylimipramine, reserpine,
6-hydroxydopamine (6-OHDA), or phentolamine
(Granata et al., 1985, 1986; Granata and Reis, 1987).
Norepinephrine
is probably not the only amine released by tyramine since tyramine causes a release of several granular amines (5-HT,
NA, DA) in synaptosomes from guinea-pig brain (Peyer et al., 1982). In this study, we tested this
hypothesis by examining the effects of tyramine and other indirectly acting sympathomimetics in the C1
area, the locus coeruleus, and
the caudal raphe nuclei, which contain adrenergic, noradrenergic, and
serotoninergic neurons,
respectively.