The perivascular adipose tissue (PVAT) is a metabolically active structure that modulates the contractile, proliferative and migratory functions of underlying smooth muscle. In normal conditions, PVAT decreases contractile responses non-specifically in various vascular beds. Alterations in the secretory properties and consequently function of PVAT occur in various cardiovascular diseases, such as hypertension and metabolic syndrome. We have previously observed that contrary to genetic or long term diet-induced obesity, in a model of short-term high fat high sucrose (HFHS) diet-induced obesity, the anti-contractile effects of PVAT were increased. Animal models of hypertension, including angiotensin II-induced hypertension, are associated with a loss of anti-contractile effects of PVAT. Thus, we hypothesized that angiotensin II-induced hypertension opposes the effects of HFHS-induced obesity on PVAT anti-contractile function. We used young control non-treated rats, HFHS obese rats, angiotensin II hypertensive rats, and AngHFHS obese hypertensive rats and compared contractile function in the absence or presence of PVAT in mesenteric resistance arteries. Systolic blood pressure was significantly increased in AngII and AngHFHS rats compared to control (AngHFHS=153±17, AngII=170±15, Con=97±6 mmHg), while not significantly different from control in HFHS rats. Visceral adipose tissue mass was overall significantly increased in HFHS and AngHFHS rats compared to control rats (e.g. retroperitoneal fat AngHFHS=0.47±0.07, HFHS=0.64±0.14, Con=0.23±0.04 % body weight). In the absence of PVAT, contractile responses to PE, 5HT and ET-1 in mesenteric artery were not altered by HFHS obesity alone, however were increased in AngII and AngHFHS conditions. Anti-contractile effects of PVAT were significantly reduced in AngII hypertension but similarly increased in HFHS and AngHFHS rats (% reduction in max contraction, con: PE=13.6, 5-HT=14.04, ET-1=19.53; HFHS: PE=13.3, 5-HT=26.13, ET-1=30.93; AngHFHS: PE=36.06, 5-HT=18.20, ET-1=39.77). These data suggest that the deleterious effects of augmented BP on PVAT function are insufficient in counteracting the increase in anti-contractile PVAT effects in response to HFHS obesity in young rats.