It was shown in this study that isolated porcine coronary arteries (PCA) contracted by depolarization with high Ko or by histamine are dose-dependently relaxed by glutamic acid, aspartic acid, N-methyl-asparate (NMDA) and γ-aminobutyric acid (GABA). Zn2+ was also shown to relax dose-dependently PCA contractions induced by 50 mM KCl with an ED50 value of about 1.5 mM and to inhibit dose-dependently histamine-induced contractions, shifting ED50 values from 6μM to 40 μM, not affecting however corresponding cumulative concentration-response (CCR) curves established for acetylcholine-induced contractions. Furthermore, since Zn2+ ions are co-localized in many glutamatergic synapses of the centralnervous system, it has been postulated in analogy to glutamate neurotoxicity that perturbationsof the synaptic zinc concentrations might be a triggering factor in several cerebral diseases, such as is chemic strokes and sustained seizures. Unfortunately, little is known so far about effects of glutamate and zinc ions on the vascular tone. Although the nature of the glutamatergic receptors occurring in the blood vessels investigated in this study remainsunclear, the results suggest that glutamate and Zn2+ ions interact with voltage-gatedas well with ligand-operated Ca-channels. An interesting aspect might be the putativerole of glutamate and zinc as long-term toxic agents in the early steps of the pathomechanisms leading to degenerative vascular lesions.