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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).
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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).
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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.
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