85 INSIGHTS INTO VAGAL GANGLIONIC SYNAPTIC INTEGRATION FROM THE VON BEZOLD-JARISCH REFLEX

Abstract

Background: The von Bezold-Jarisch reflex (vBJR) elicits a vagally-mediated, cardioprotective bradycardia, which is attenuated in hypertensive models1. The cardiac ganglia gate vagal drive and impaired ganglionic signal transmission is also found in hypertensive models2. We therefore extended our recent intracellular study of cardiac vagal ganglion neurone (CVN) responses to cardiorespiratory reflexes3 to include the vBJR. Methods: Intracellular recordings were made from CVNs in the working heart-brainstem preparation of Wistar rats (P18-25, n = 6). They were classified as tonic or phasic based on their firing responses. We compared their response to vBJR activation using phenylbiguanide (PBG, 200/ug i.a.) with baro-, chemo- and diving reflex responses. Results: PBG produced robust bradycardias (-98 ± 29bpm). Tonic cell (n = 4) EPSP and spike rates were increased by activation of all reflexes indicating convergence through a single population of CVNs. Strikingly, the increase in EPSP/spike frequency was ∼2.5x higher during the vBJR than the chemoreflex (16 ± 10 vs 7 ± 4 Hz, n = 4), despite similar bradycardias (-98 ± 29 vs -98 ± 35bpm). PBG-responses depended on intact brainstem function, and no evidence of direct depolarisation or activation of local cardiac ganglionic circuits was found. PBG never excited phasic cells (putative interneurones, n = 10). Conclusions: vBJR activation excites a common pool of vagal postganglionic neurones shared with the other cardiorespiratory reflexes. The relatively augmented excitation of CVNs by the vBJR means that the intrinsic integrative properties of the ganglion cells are important in determining the magnitude of end organ response and thus changes at the level of the ganglion may play a role in its depression in hypertension.