Established dogma is that sympathomimetic amines, including β-phenylethylamine (PEA), increase blood pressure by releasing noradrenaline from sympathetic neurons. Recent evidence allowing longer contact with isolated immersed tissues indicates other mechanisms. The present study re-evaluates the mechanism of pressor responses to PEA in anaesthetised rats with longer exposure to infusions. Blood pressure and heart rate were monitored by cannulating a common carotid artery of anaesthetised male Sprague-Dawley rats. Drugs were administered by bolus doses or by 20-min infusions via a cannulated jugular vein. Increases in blood pressure by bolus doses of the α-adrenoceptor agonist, phenylephrine, were converted to depressor responses by prazosin and therefore α-adrenoceptor-mediated. Pressor responses to bolus doses of PEA were reduced. PEA infusions yielded four-phase responses: An initial increase in pressure (phase 1) blocked by prazosin was due to α-adrenoceptor vasoconstriction and a secondary fall in pressure (phase 2) due to vasodilatation by nitric oxide release. A later pressure increase (phase 3), further elevated after infusion stopped (phase 4), was not attenuated by prazosin and therefore non-adrenergic. This study showed for the first time that the sympathomimetic amine, β-phenylethylamine, increases blood pressure by two mechanisms. The established indirect sympathomimetic mechanism applies to bolus dose administration. However, with prolonged exposure to infusions, an additional slow-onset sustained non-adrenergic blood pressure increase occurs, most likely mediated via trace amine-associated receptors (TAAR-1). This response will dominate with prolonged exposures in clinical practice. These results prompt a re-evaluation of established dogma on the indirect sympathomimetic mechanisms of these amines.