The bed nucleus of the stria terminalis (BST) has been known to contain estrogen (E)-concentrating neurons. In addition, injections of E into BST have been reported to potentiate the sympathoinhibitory arterial pressure (AP) and heart rate (HR) responses elicited by glutamate (Glu) stimulation. In this study, the effect of glutamate antagonist receptors in the rostral ventrolateral medulla (RVLM) on the cardiovascular responses to Glu stimulation of BST (0.25 M; 20 nl) was investigated in the chloralose anaesthetized, ovariectomized (OVX; n=6) or OVX+E-treated (30 pg/ml plasma E; n=10) female Wistar rats. Glu stimulation of the BST decreased AP (-15 ± 5 mmHg) and HR (-25.23± 2 bpm) in the OVX+E animals and in OVX only animals (AP, -29.78 ± 4.17 mmHg; HR, -17.3 ± 3.1 bpm). Microinjection of glutamate antagonist receptors, kynurenic acid (5.0 mM, 100nl) into the ipsilateral RVLM reversibly attenuated glutamate-induced bradycardi and depressor responses to BST stimulation in OVX only animals (OVX; n=8 AP,-13.7±2.6 and HR,-8.1±4.3) but in OVX+E animals only attenuated glutamate induced bradycardia, but not depressor response (OVX+E;n=7 AP,-11.7±3.8 and HR, -16.7±2.3). These data suggest that RVLM sympathetic premotor neurons contain glutaminergic receptors mediate the sympathoinhibitory responses to stimulation of BST in OVX animals.