To elucidate the role of the rostral veetrolateral medulla (RVLM) in cardiovascular control through the release of central amino acid neurotransmitters, experiments were per-formed in Sprague-Dawtey (normotensive) rats and spontane-ously hypertensive rats (SHR) anesthetized with urethane by using microdialysis sampling from the RVLM for determination of amino acid neurotransmitters. The baseline release of the excitatory amino acid neurotransmitter, glutamate (GLU) from the RVLM in SHR was higher and these of the inhybit cry amino acid neurotransmitters, glycine (GLY), taurine (TAU), and y-aminobutyric acid (GABA), were lower than in normotensive rats. Microinjection of angiotensin ll (ANG Ⅱ) into the RVLM caused a dose-dependent increase in mean arterial pressure (MAP) and heart rate (HR), accompanied by increased release of GLU in the RVLM. In contrast, microinjection of the ANG ll type 1 receptor (AT1) antagonist CV 11974 into the RVLM reduced MAP and HR, accompanied by increased release of GLY, TAU and GABA. These changes in MAP and HR after administration of ANG ll or AT, antagonist were partially blacked by the use of the corresponding antagonist of each amino acid neurotrans-mitter. Furthermore, these effects were more prominently seen in SHR than in normotensive rats. These results suggest that the release of amino acid neurotransmitters mediate the cardiovaseutar effects of the aag[otensin system in the RVLM, which may be involved in the generation of hypertension in SHR.