The goal of this study was to determine the dependence of the acute hypertensive response to a novel model of acute psychosocial stress on the sympathetic and renin-angiotensin systems. Baseline MAP, HR and locomotor activity were measured with telemetry in mice for a 1 hour period and averaged 98 ± 1 mmHg, 505 ± 3 bpm and 5 ± 1 counts, respectively. Stress was induced by placing a mouse into a cage previously occupied by a different male mouse, and this increased MAP, HR and activity in the control group by 40 ± 2 mmHg, 204 ± 25 bpm and 68 ± 6 counts, respectively. Each measure gradually returned to baseline levels by 90 minutes after beginning cage switch. Pre-treatment with terazosin (10 mg/kg, i.p.) significantly reduced the initial increase in MAP to 12 ± 6 mmHg, while MAP for the last 45 minutes was superimposable on control values. Atenolol (10 mg/ml) had no effect to blunt the initial increase in MAP but had a growing effect from 10 minutes onward, decreasing MAP all the way to baseline by 60 minutes after starting cage switch. Captopril (2 mg/mL) treatment caused a very similar response. All 3 treatments significantly decreased the area under the blood pressure curve, and the blood pressure effect could not be attributed uniformly to effects on heart rate or activity. These data suggest that our novel model of psychosocial stress causes an initial ₁ receptor-dependent increase in MAP. The later-phase of the pressor response is blocked similarly by a ₁ receptor antagonist and an ACE inhibitor, independent of heart rate, suggesting that the ₁-dependent blood pressure effect is due in large part to the renin-angiotensin system.