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Acetylcholine (Ach) causes vasodilatation by nitric oxide (NO) release from the vascular endothelium. Vasoconstrictors such as α-adrenoceptor agonists (phenylephrine) or thromboxane TxA 2 mimetics (U46619) also release endothelial NO. Inhibition of nitric oxide synthase (NOS) with N ω -nitro-L-arginine (L-NAME) potentiates vasoconstriction by phenylephrine and the trace amine, β-phenylethylamine (PEA), indicating underlying opposing vasodilatation. However, the roles of the endothelium and NO in vasodilator and constrictor responses of guinea-pig aorta have not been examined and are the subject of this study. Guinea-pig thoracic aorta rings were set up in aerated Krebs solution (37 °C) and isometric tension recorded. Contractions to phenylephrine were fast onset, rapidly waned and antagonised by prazosin. PEA contractions were slow onset, sustained and not antagonised by prazosin and therefore not α 1 -adrenoceptor-mediated. PEA and phenylephrine contractions were enhanced by L-NAME whether endothelium was present or not. Ach produced only weak relaxation in a small proportion of endothelium intact U46619-constricted aortae, which were abolished by endothelium removal. In uncontracted aortae Ach caused small contractions, which like PEA contractions were potentiated by endothelium removal. α-Adrenoceptor agonists and trace amines release NO from non-endothelial sites causing underlying opposing vasodilatation. The endothelium plays only a minor role in vasodilator and vasoconstrictor responses of guinea-pigs aorta., (Copyright © 2019 Elsevier Inc. All rights reserved.)