Objective: To examine the exact profile of expression and to determine the functional significance of the angiotensin II (Ang II), type 1 (AT₁) and type 2 (AT₂) receptors during rat aortic development and following rat carotid artery balloon injury. Methods: AT₁ and AT₂ mRNA levels in rat aortae were measured using a quantitative reverse transcription polymerase chain reaction technique. Ang II receptor function was assessed by quantitating the effects of AT₁ (DuP753) and AT₂ (PD123319) receptor antagonists during these processes. Results: During aortic development, AT₁ expression was detected on gestational day 14, increased until embryonic day 16 (E16), after which, levels were similar throughout postnatal development. Conversely, AT₂ mRNA first appeared at E16, reached maximal levels between E19 and neonatal day 1, and decreased thereafter. DNA synthesis rates decreased with aortic development (high at E15, 73.8±3.1%; dropping to 37.5±2.3% by E21). Whereas AT₁ receptor antagonism accelerated this developmentally regulated decrease in DNA synthesis, AT₂ receptor antagonism blunted this decrease. Because activated adult medial smooth muscle cells express a neonatal phenotype after vascular injury, we assessed Ang II receptor levels and function after carotid artery balloon injury. Both receptor subtypes increased; however, AT₂ receptor mRNA expression peaked earlier than AT₁ (48 to 72 h after injury). As with aortic development, DNA synthesis occurring between 24 to 48 h after injury (when AT₂ receptors constitute 10% of the Ang II receptor population) decreased in DuP753-treated animals and increased in PD123319-treated animals. Conclusion: These results indicate that Ang II receptors play a role in vascular development by promoting opposing effects on vascular smooth muscle cell growth.