This study demonstrates that SA and AV nodal pacemaker activity and AV conductivity are controlled multi-directionally by intracardiac sympathetic nerves, in contrast with parasympathetic nerves.
Stimulation of discrete intracardiac sympathetic nerves to the SA (SAS stimulation) or AV nodal region (AVS stimulation) increased the heart rate or decreased AV conduction time and caused an AV junctional rhythm, respectively, in anesthetized dogs treated with atropine. Topical application of tetrodotoxin (TTX) at the SAS or AVS stimulation locus totally inhibited the response to each stimulation, whereas each TTX treatment slightly attenuated the chronotropic response to the right ansa stimulation by 23 ± 7.7% and the dromotropic response to the left ansa stimulation by 7 ± 7.5%. TTX abolished AVS stimulation-induced one. Before atropine, topical application of hexamethonium at the locus for stimulation of intracardiac parasympathetic nerves to the SA (SAP stimulation) or AV nodal region (AVP stimulation) abolished almost totally negative chronotropic responses to SAP and cervical vagus stimulation or negative dromotropic responses to AVP and cervical vagus stimulation, respectively. These results demonstrate that activation of a very small population of intracardiac sympathetic nerves to target cells is enough to induce positive chronotropic and dromotropic responses in the heart in situ, and that SA and AV nodal pacemaker activity and AV conductivity are controlled multi-directionally by intracardiac sympathetic nerves in contrast with parasympathetic ones.
Furukawa et al. (Tue,) studied this question.
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