Proceedings of The Physiological Society

University College Cork (2004) J Physiol 560P, C8



Pickering,Anthony ; Simms,Annabel E; Paton,Julian FR;

1. Anaesthesia, University of Bristol, Bristol, United Kingdom. 2. Physiology, University of Bristol, Bristol, United Kingdom.

The arterial baroreflex receives its afferent input from sensors located in the carotid bifurcation and aortic arch. In this study we examined the role of the individual afferent sites in determining the overall baroreflex response. Studies were performed using decerebrate, artificially perfused rats (Pickering et al., 2003). Briefly, Wistar rats (90g) were anaesthetised with Halothane until loss of paw withdrawal reflex and the intestines were removed. The animal was decerebrated precollicularly and perfused, with a carbogenated Ringers solution. Sympathetic nerve activity was recorded from the greater splanchnic nerve and the thoracic chain. For the isolated carotid sinus experiments a double lumen cannula was inserted into the common carotid and connected to a separate perfusion circuit. Data are mean±sem. Systemic perfusion pressure ramps demonstrated baroreflex sympathoinhibition and bradycardia. By isolating one carotid sinus and applying pressure ramps we showed baroreflex sympathoinhibition, apnoea and vascular resistance changes. However, despite vigorous pressure stimulation (up to 200mmHg, n=8), we were unable to evoke baroreflex bradycardias. Direct injection of sodium cyanide (20ug) to the isolated carotid sinus provoked a chemoreflex response indicating that the sinus nerve was intact. We therefore undertook a series of baroreceptor denervations, sequentially cutting the afferent nerves from the aortic arch (aortic depressor, ADN) and the carotid sinus (glossopharyngeal). Irrespective of the order of denervation we were able to demonstrate pronounced sympathoinhibition from a single baroreceptor site (figure, n=9). In contrast cutting a single ADN was sufficient to reduce the cardiac gain by 85% and section of the contralateral nerve completely abolished the bradycardia (gain from -2.6±0.5 to 0±0.09bpm/mmHg, n=6). The cardiac baroreflex appeared unchanged by loss of input from the carotids (n=5). These data indicate the aortic arch inputs in the rat predominate in mediating the cardiac baroreflex. The sympathetic component of the baroreflex was less sensitive to the sequential loss of afferent inputs. These different response properties explain our difficulty (and that of others (Dworkin et al., 2000)) in obtaining a bradycardia from the isolated carotid sinus. This may give some functional significance to the differential target distribution, within the nucleus of the solitary tract, of baroafferents carried from the aortic arch versus the carotid sinus (Chan et al., 2000).

Where applicable, experiments conform with Society ethical requirements