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.