The action of the peptide YPVQPFTE, isolated from the tryptic hydrolysate of γ-casein, displays a bradykinin potentiating activity, characterized by the arterial blood pressure recording analysis. The intravenous injection of bradykinin (0.5μg) pre-treated with this peptide (30μg) was performed by chronic assay in conscious spontaneously hypertensive rats (SHR) and also by acute assay in normotensive Wistar rats, anaesthetized by three currently used anaesthetic drugs: sodium pentobarbitone (68mg/kg, i.p.); ketamine hydrochloride (25mg/kg, i.p.) associated with xylazine hydrochloride (10mg/kg, i.p.) and atropine (0,05mg/Kg, i.p.); and chloral hydrate (160mg/kg, i.p.). The peptide displayed bradykinin potentiating activity, by means that was not related to angiotensin converting enzyme (ACE) inhibition. The hypotensive areas were compared by two parameters, namely magnitude decrease (mmHg) and time course (min) to recover the pressure baseline values. In the first parameter, conscious SHR presented a greater decrease of the arterial blood pressure, followed by chloral hydrate and sodium pentobarbitone, ketamine–xylazine, which presented a small decrease. For the time parameter, the two depressants of the CNS presented the higher time to recover from the hypotension and ketamine–xylazine association resulted similar to conscious SHR group. The results demonstrated that the magnitude of the hypotension (mmHg) caused by the action of the vasoactive compounds was not directly altered by anaesthetic drugs even with compounds not related to ACE but the time to recover from this hypotension was significantly different depending on pharmacological mechanism proprieties of the anaesthetic agent used, suggesting that the main effects observed in this case is the failure to recover basal Mean Arterial Pressure (MAP) in the presence of depressant of the central nervous system.