risch reflex attenuates dynamic gain of baroreflex neural arc. Am J Physiol Heart Circ Physiol 285: H833-H840, 2003. First published April 24, 2003 10.1152/ajpheart.01082. 2002-Although acute myocardial ischemia or infarction may induce the Bezold-Jarisch (BJ) reflex through the activation of serotonin receptors on vagal afferent nerves, the mechanism by which the BJ reflex modulates the dynamic characteristics of arterial pressure (AP) regulation is unknown. The purpose of this study was to examine the effects of the BJ reflex induced by intravenous phenylbiguanide (PBG) on the dynamic characteristics of the arterial baroreflex. In seven anesthetized rabbits, we perturbed intracarotid sinus pressure (CSP) according to a white noise sequence while renal sympathetic nerve activity (RSNA), AP, and heart rate (HR) were recorded. We estimated the transfer function from CSP to RSNA (neural arc) and from RSNA to AP (peripheral arc) before and after 10 min of intravenous administration of PBG (100 g ⅐ kg Ϫ1 ⅐ min Ϫ1 ). The intravenous PBG decreased mean AP from 84.5 Ϯ 4.0 to 68.2 Ϯ 4.7 mmHg (P Ͻ 0.01), mean RSNA to 76.2 Ϯ 7.0% (P Ͻ 0.05), and mean HR from 301.6 Ϯ 7.7 to 288.4 Ϯ 9.0 beats/min (P Ͻ 0.01). The intravenous PBG significantly decreased neural arc dynamic gain at 0.01 Hz (1.06 Ϯ 0.08 vs. 0.59 Ϯ 0.17, P Ͻ 0.05), whereas it did not affect that of the peripheral arc (1.20 Ϯ 0.12 vs. 1.18 Ϯ 0.41). In six 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 BJ 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. renal sympathetic nerve activity; transfer function; systems analysis; rabbits; carotid sinus baroreflex THE CIRCULATORY SYSTEM has several mechanoreceptors and chemoreceptors in a variety of regions. The cardiopulmonary region is rich in such receptors. The most vagal afferent fibers from the cardiopulmonary receptors to the vasomotor center are classified as C fibers.Activation of the cardiopulmonary chemosensitive vagal afferent fibers reduces arterial pressure (AP), heart rate (HR), and cardiac output (31). These responses, mediated by 5-hydroxytryptamine (5-HT 3 ) serotonergic receptors on the cardiopulmonary vagal afferent fibers, are known as the Bezold-Jarisch (BJ) reflex (2, 7, 32). Although its physiological importance remains debatable, the BJ reflex could play a significant role in developing pathological responses associated with acute myocardial ischemia (19,20,24). Elucidating the effects of the BJ reflex on the circulatory regulation would be useful for better understanding the pathophysiology of ischemic heart diseases (16, 27). The BJ reflex can be induced chemically with pharmacological agents such as 5-HT and ...