The arterial baroreflex system is one of the most important negative-feedback systems that stabilizes arterial pressure (AP) against exogenous pressure perturbation. The arterial baroreflex may be divided into the neural and peripheral arc subsystems [1][2][3]. The neural arc represents the signal transduction pathway from baroreceptor pressure input to efferent sympathetic nerve activity (SNA). The peripheral arc represents the regulatory pathway from SNA to AP. Static characteristics of the two arcs provide information on the operating point of AP regulation [2,4]. The dynamic characteristics of the two arcs determine the stability and quickness of AP regulation [1,5]. Because the baroreflex operates dynamically under the ordinary conditions of daily activity, changes in baroreflex dynamic characteristics critically affect the performance of AP regulation and consequently have an impact on quality of life. An assessment of baroreflex dynamic characteristics in conjunction with altered hormonal regulation of the cardiovascular sys- Key words: renal sympathetic nerve activity, transfer function, systems analysis, rabbits, carotid sinus baroreflex.Abstract: Although the elevation of angiotensin II (Ang II) associated with cardiovascular diseases has been considered to suppress the arterial baroreflex function, how Ang II affects dynamic arterial pressure (AP) regulation remains unknown. The aim of the present study was to elucidate the acute effects of Ang II on dynamic AP regulation by the arterial baroreflex. In seven anesthetized Japanese white rabbits, we randomly perturbed intra-carotid sinus pressure (CSP) according to a binary white noise sequence while recording renal sympathetic nerve activity (RSNA) and AP. We estimated the neural arc transfer function from CSP to RSNA and the peripheral arc transfer function from RSNA to AP before and after 30-min intravenous administration of Ang II (100 ng/kg/min). Ang II increased mean
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