Hemodynamic responses to angiotensin II and the role of AT₁ and AT₂ receptors and the autonomic nervous system in mediating acute responses to angiotensin II were investigated in anesthetized CD1 mice. Injections of angiotensin II caused dose-related increases in systemic arterial pressure that were antagonized by candesartan. Pressor responses to angiotensin II were not altered by PD-123,319 in doses up to 25 mg/kg iv. At the lowest dose studied (20 μg/kg iv), the inhibitory effects of candesartan were competitive, whereas at the highest dose (100 μg/kg iv) the dose-response curve for angiotensin II was shifted to the right in a nonparallel manner with inhibitory effects that could not be surmounted. The inhibitory effects of candesartan were selective and were similar in animals pretreated with enalaprilat (1 mg/kg iv) to reduce endogenous angiotensin II production. Acute pressor responses to angiotensin II were not altered by propranolol (200 μg/kg iv), phentolamine (200 μg/kg iv), or atropine (1 mg/kg iv) but were enhanced by hexamethonium (5 mg/kg iv). Increases in total peripheral resistance induced by angiotensin II were inhibited by the AT₁-receptor antagonist but were not altered by AT₂-, α-, or β-receptor antagonists. These results suggest that acute pressor responses to angiotensin II are mediated by AT₁ receptors, are buffered by the baroreceptors, and are not modulated by effects on AT₂ receptors and that activation of the sympathetic nervous system plays little if any role in mediating rapid hemodynamic responses to the peptide in anesthetized CD1 mice.