Cardiopulmonary baroreceptors affect reflexive startle eye blink S. Richter a, ⁎, A. Schulz a , J. Port b , T.D. Blumenthal c , H. Schächinger a a Division of Clinical Physiology, Institute of Psychobiology, University of Trier, Trier, Germany b Institute of Medical Technology, University of Stuttgart, Stuttgart, Germany c Department of Psychology, Wake Forest University, Winston-Salem, North Carolina, USA abstract article info Article history: Received 19 February 2009 Received in revised form 12 August 2009 Accepted 18 September 2009 Keywords: Acoustic startle reflex Arterial baroreceptors Cardiopulmonary baroreceptors Lower body negative pressure Reaction time Baroafferent signals originating from the ‘high pressure’ arterial vascular system are known to impact reflexive startle eye blink responding. However, it is not known whether baroafferent feedback of the ‘low pressure’ cardiopulmonary system loading status exerts a similar effect. Lower Body Negative Pressure (LBNP) at gradients of 0, -10, -20, and -30 mm Hg was applied to unload cardiopulmonary baroreceptors. Acoustic startle noise bursts were delivered 230 and 530 ms after spontaneous R-waves, when arterial baroreceptors are either loaded or unloaded. Eye blink responses were measured by EMG, and psychomotor reaction time by button pushes to startle stimuli. The new finding of this study was that unloading of cardiopulmonary baroreceptors increases startle eye blink responsiveness. Furthermore, we replicated the effect of relative loading/unloading of arterial baroreceptors on startle eye blink responsiveness. Effects of either arterial or cardiopulmonary baroreceptor manipulations were not present for psychomotor reaction times. These results demonstrate that the loading status of cardiopul- monary baroreceptors has an impact on brainstem-based CNS processes. © 2009 Elsevier Inc. All rights reserved. 1. Introduction There is growing evidence that neural visceral afferent signals have an impact on higher central nervous system (CNS) processes, such as emotion and cognition [1,2]. Many of the afferent signals, which ascend via vagal, glossopharyngeal, and thoracic afferent nerve fibers, originate from phasically active thoracic or abdominal structures, such as the lungs, gastrointestinal organs, and the central cardiovascular system [3]. Visceral afferents play an important role in adaptation and homeostasis, and neural baroreceptor feedback is required for controlling heart rate, blood pressure, cardiac workload, and vascular resistance, but has also been found to affect central nervous system (CNS) functions which are not directly linked to cardiovascular regulation, such as pain processing [4]. Baroreceptors are located in arterial vessel walls of the aortic arch and the carotid sinus (the high pressure system), but also in pulmonary vessels and atria (the cardiopulmonary low pressure system). Due to their distribution and due to the blood vessel wall characteristics, arterial baroreceptors respond to changes in arterial pressure, whereas cardiopulmonary baroreceptors respond to changes in central venous pressure which, during healthy conditions, is proportional to changes in central venous volume. Loading of baroreceptors enhances their neural output, unloading induces the opposite effect. The CNS structures prominently involved in both baroreflex pathways are located in the brainstem. Information from arterial and cardiopulmonary baroreceptors converges in the nucleus tractus solitarii (NTS), and is further relayed to the nucleus ambiguous and the ventrolateral medulla [5–8]. Both baroreceptor systems project, via the NTS, to similar CNS structures (e.g., Anterior cingulum, Insular cortex, Locus coeruleus) which have been shown to be involved in pain processing, emotion, and regulation of higher cognitive–motor functions [9–11]. Several psychophysiological effects of loading or unloading arterial baroreceptors have been described. Enhanced arterial baroreflex afferent feedback activity impacts on EEG activity [12,13], attenuates pain perception [13–18], and induces a prolongation of psychomotor reaction times [12,19,20], and unloading vs. loading of arterial baroreceptors may affect memory processes [21]. Furthermore, neural arterial baroreceptor afferent feedback transmission has an inhibitory effect on simple brainstem reflexes, such as the startle response [22– 25]. The startle eye blink reflex is a protective reflex, which is reliably evoked by presentation of abrupt and intense acoustic noise stimuli. This reflex is affected by spontaneous neural arterial baroreceptor afferent feedback transmission, since lower startle responsiveness was found when stimuli were presented during the early cardiac cycle phase, when arterial baroreceptors are loaded, as compared to the late cardiac cycle phase, when arterial baroreceptors are relatively unloaded. This effect relies on intact neural afferent signal transmis- sion, and it is absent in diabetic autonomic neuropathy [24]. However, in contrast to arterial baroreceptors, relatively little is known about the significance of cardiopulmonary baroreceptors for Physiology & Behavior 98 (2009) 587–593 ⁎ Corresponding author. Division of Clinical Physiology, Institute of Psychobiology, University of Trier, Johanniterufer 15, D-54290 Trier, Germany. Tel.: +49 6512013735; fax: +49 6512013737. E-mail address: richters@uni-trier.de (S. Richter). 0031-9384/$ – see front matter © 2009 Elsevier Inc. All rights reserved. doi:10.1016/j.physbeh.2009.09.010 Contents lists available at ScienceDirect Physiology & Behavior journal homepage: www.elsevier.com/locate/phb