ABLATION OF POSTERIOR ATRIAL GANGLIONATED PLEXUS POTENTIATES SYMPATHETIC TACHYCARDIA TO BEHAVIORAL STRESS

The role of the posterior atrial ganglionated plexus (PAGP) in heart r ate (HR) control was tested in unanesthetized dogs (n = 8). Resting HR was unchanged before (85 +/- 20 beats/min, mean +/- SD) versus after (87 +/- 18 beats/min) surgical ablation of these intrinsic cardiac gan glia (PAGPX). However, the peak tachycardia to a 30-s stressful stimul us was significantly increased (P < 0.05) from +53 +/- 22 beats/min be fore the denervation to +77 +/- 13 beats/min after PAGPX Conversely, t he peak HR increase during the stress after P-adrenergic blockade was the same before (36 +/- 24 beats/min) versus after (38 +/- 14 beats/mi n) PAGPX. Moreover, the HR response to a neutral behavioral stimulus, which is mediated primarily by withdrawal of parasympathetic inhibitio n of the sinoatrial (SA) node, was unaltered by PAGPX. Thus the augmen ted tachycardia subsequent to PAC;PX was attributable primarily to inc reased sympathetic action at the SA node. These findings indicate that a major role of PAGP parasympathetic neurons is to inhibit sympathoex citatory effects on HR, probably either via interactions between neuro ns comprising the intrinsic plexus(es) or perhaps via presynaptic inhi bition of sympathetic neurotransmitter release; This organization woul d allow parasympathetic ganglia within the PAGP to selectively modify sympathetic input to the SA node independent of direct vagal inhibitio n of pacemaker activity.