Interaction between cardiac receptors and sinoaortic baroreceptors in the control of efferent cardiac sympathetic nerve activity during myocardial ischemia in dogs.

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Abstract
The relative influence of arterial baroreceptors and of cardiac receptors with vagal afferents on efferent cardiac sympathetic nerve activity during coronary artery occlusion was determined. Changes in heart rate (beats/min), arterial pressure (mm Hg), and integrated cardiac sympathetic nerve activity (CSNA, percent change from control; recorded from the cut central end of the left ventral ansa subclavia) were determined during transient (90-s) circumflex (Cx) and anterior descending (LAD) coronary artery occlusions. In dogs with carotid and aortic baroreceptors intact, increases (mean .+-. SE) in CSNA during Cx (7 .+-. 2%) and LAD (9 .+-. 5%) occlusions were similar despite a significantly greater fall in arterial pressure during Cx (-14 .+-. 3 mm Hg) than during LAD (-5 .+-. 2 mm Hg) coronary artery occlusion. Heart rate did not change during these occlusions. In 3 dogs, hypotension induced by inferior vena caval occlusion resulted in greater increases in CSNA than did comparable decreases in arterial pressure resulting from occlusion of LAD or Cx. In dogs with sinoaortic denervation, Cx coronary occlusion resulted in decreases in CSNA (-14 .+-. 4%), arterial pressure (-38 .+-. 6 mm Hg), and heart rate (-13 .+-. 5 beats/min), whereas LAD occlusion resulted in a small decrease in arterial pressure (-12 .+-. 5 mm Hg) and no change in CSNA or heart rate. Vagotomy abolished the decreases in CSNA and heart rate and attenuated the arterial pressure responses to Cx occlusion. Cardiac receptors with vagal afferents exert an inhibitory influence on cardiac sympathetic nerve activity during myocardial ischemia, particularly during inferoposterior ischemia and this influence limits the arterial baroreceptor-mediated increases in CSNA resulting from ischemia-induced hypotension.