Abstract

Ablation of posterior atrial ganglionated plexus potentiates sympathetic tachycardia to behavioral stress. Am. J. Physiol. 275 (Regulatory Integrative Comp. Physiol. 44): R779–R787, 1998.—The role of the posterior atrial ganglionated plexus (PAGP) in heart rate (HR) control was tested in unanesthe-tized dogs (n 5 8). Resting HR was unchanged before (85 6 20 beats/min, mean 6 SD) versus after (87 6 18 beats/min) surgical ablation of these intrinsic cardiac ganglia (PAGPX). However, the peak tachycardia to a 30-s stressful stimulus was significantly increased (P, 0.05) from 153 6 22 beats/min before the denervation to 177 6 13 beats/min after PAGPX. Conversely, the peak HR increase during the stress after b-adrenergic blockade was the same before (36 6 24 beats/min) versus after (38 6 14 beats/min) PAGPX. More-over, the HR response to a neutral behavioral stimulus, which is mediated primarily by withdrawal of parasympathetic inhibition of the sinoatrial (SA) node, was unaltered by PAGPX. Thus the augmented tachycardia subsequent to PAGPX was attributable primarily to increased sympathetic action at the SA node. These findings indicate that a major role of PAGP parasympathetic neurons is to inhibit sympatho-excitatory effects on HR, probably either via interactions between neurons comprising the intrinsic plexus(es) or per-haps via presynaptic inhibition of sympathetic neurotransmit-ter release. This organization would allow parasympathetic ganglia within the PAGP to selectively modify sympathetic input to the SA node independent of direct vagal inhibition of pacemaker activity. intrinsic cardiac ganglia; sinoatrial node; pacemaker func-tion; autonomic nervous system; vagus nerve; classical (Pav-lovian) conditioning