We determined the effect produced by microinjection of Ang-(1-7) and Ang II into two key regions of the medulla for the control of the circulation, the rostral and caudal ventrolateral medulla (RVLM and CVLM, respectively), on the baroreflex control of heart rate in anesthetized rats. Reflex bradycardia and tachycardia were induced by increases and decreases in mean arterial pressure (MAP) produced by intravenous phenylephrine and sodium nitroprusside, respectively. The pressor effects of Ang-(1-7) or Ang II (25 pmol) after RVLM microinjection (11±0.8 and 10±2 mmHg, respectively) were not accompanied by consistent changes in HR. In addition, RVLM microinjection of these angiotensin peptides did not alter the bradycardic or the tachycardic component of the baroreflex. CVLM microinjections of Ang-(1-7) or Ang II produced hypotension (-11±1.5 and -11±1.9 mmHg, respectively) that was also not accompanied by significant changes in HR. However, CVLM microinjections of angiotensins induced differential changes in the baroreflex control of HR. Ang-(1-7) attenuated the baroreflex bradycardia (0.26±0.06 vs 0.42±0.08 ms/ mmHg, before) and facilitated the baroreflex tachycardia (-0.86±0.19 vs -0.42±0.10 ms/ mmHg, before), Ang II produced the opposite effect, attenuating the tachycardia (-0.09±0.06 vs -0.31±0.07 ms/ mmHg, before) and facilitating the baroreflex bradycardia (0.67±0.16 vs 0.41±0.05 ms/ mmHg, before). The modulatory effect of Ang II and Ang-(1-7) on baroreflex sensitivity was completely abolished by peripheral administration of methyl-atropine. These results suggest that Ang II and Ang-(1-7) at the CVLM produce a differential modulation of the baroreflex control of heart rate, probably through distinct effects on the parasympathetic drive to the heart.