This study tested the hypothesis that baroreceptor vagal reflex (BVR) attenuation in developing rats, which occurs between postnatal ages (P) of 10 to 20 days old, is due to a central action of angiotensin II (Ang II). In urethane or halothane anaesthetised mature (P > 45) or pre-weaned rats (P14-18), BVR sensitivity was estimated as the ratio between the fall in heart rate and the increase in arterial pressure induced by i.v. phenylephrine. An Ang II AT1 receptor antagonist, losartan, was administered intra-venously (i.v.) or microinjected into brainstem structures. In pre-weaned rats BVR sensitivity was increased significantly by losartan (5 mg/kg; urethane anaesthesia: p < 0.01; halothane anaesthesia: p < 0.05) while a larger dose (10 mg/kg) was ineffective in mature animals. In pre-weaned rats, microinjection of losartan (500 pmol) into the nucleus tractus solitarii (NTS) but neither area postrema nor subjacent nuclei, reversibly increased the sensitivity of BVR (+89 +/- 19%; p < 0.01, n = 12). Microinjection of losartan (500 or 1500 pmol) into the NTS of mature rats did not change the BVR. An AT2-antagonist, PD123-319 did not restore the BVR sensitivity in pre-weaned rats. Thus, AT1 receptors located within the NTS play a pivotal role in the developmental attenuation of the BVR in pre-weaned rats.