Although acute myocardial ischemia or infarction may induce the Bezold-Jarisch (B-J) reflex through the activation of 5-HT₃ receptors on vagal afferent nerves, the mechanism by which the B-J reflex modulates the dynamic characteristics of arterial pressure (AP) regulation remains unknown. The purpose of the present study was to examine the effects of the B-J reflex induced by intravenous phenylbiguanide (PBG) on the dynamic characteristics of the arterial baroreflex. In 7 anesthetized rabbits, we perturbed intra-carotid sinus pressure (CSP) according to a white noise sequence while recording renal sympathetic nerve activity (RSNA), AP, and heart rate (HR). We estimated the transfer function from CSP to RSNA (neural arc) and from RSNA to AP (peripheral arc) before and after 10-min intravenous administration of PBG (100 µg/kg/min). The intravenous PBG decreased mean AP from 84.5 ± 4.0 to 68.2 ± 4.7 mmHg (P < 0.01), mean RSNA to 76.2 ± 7.0 % (P < 0.05) and mean HR from 301.6 ± 7.7 to 288.4 ± 9.0 beats/min (P < 0.01). The intravenous PBG significantly decreased neural arc dynamic gain at 0.01 Hz (1.06 ± 0.08 vs. 0.59 ± 0.17, P < 0.05), whereas it did not affect that of the peripheral arc (1.20 ± 0.12 vs. 1.18 ± 0.41). In 6 different rabbits without intravenous PBG, the neural arc transfer function did not change between two experimental runs with intervening interval of 10 min, excluding the possibility that the cumulative effects of anesthetics had altered the neural arc transfer function. In conclusion, excessive activation of the B-J reflex during acute myocardial ischemia may exert an adverse effect on AP regulation, not only by sympathetic suppression, but also by attenuating baroreflex dynamic gain.