ANG II alters the short-term blood pressure buffering capacity of the baroreflex in many adult animals. In embryonic chickens, high plasma ANG II levels contribute to baseline mean arterial pressure (MAP, kPa) without changing heart rate (ƒH, beats/min). We hypothesized, on the basis of these features, that an ANG II-induced reduction in baroreflex sensitivity is present in embryonic chickens as in adults. We examined baroreflex function in day 19 embryonic chickens (Gallus gallus domesticus) after chronic depletion of endogenous ANG II via angiotensin-converting enzyme (ACE) inhibition with captopril (5 mg/kg) from days 5-18 of incubation. The correlation between MAP and ƒH was assessed using increasing doses of sodium nitroprusside, a vasodilator, and phenylephrine, a vasoconstrictor. We used two analytical methods to evaluate baroreflex function: a conventional "static" method, in which maximal MAP and ƒH responses were examined, and a "dynamic" method that assessed beat-to-beat changes during the response to pharmacological manipulation. Captopril-treated embryos were hypotensive by 19% with baroreflex slopes ∼40% steeper and normalized gains ∼50% higher than controls, and differences across treatments were similar using either analytical method. Furthermore, reintroduction of ANG II via infusion raised MAP back to control levels and decreased the baroreflex gain in captopril-treated embryos. Therefore, during typical chicken development, ANG II dampens the baroreflex regulatory capacity and chicken embryos can be used as a natural model of elevated ANG II for studying developmental cardiovascular function. This study is the first to demonstrate that reduction of embryonic ANG II alters normal baroreflex function.