Abstract

In separate sets of experiments, we observed that activation of left ventricular sympathetic afferents by transmural myocardial ischemia (TMI) appeared to elicit greater reflex increases in efferent sympathetic nerve activity (SNA) to the heart than to the kidney. To assess this observation more rigorously, we simultaneously measured changes in cardiac and renal SNA elicited by TMI and by epicardial and intracoronary bradykinin (BK). Experiments were performed in 19 chloralose-anesthetized dogs with sinoaortic denervation and vagotomy. TMI was created by a 2 min complete occlusion of the anterior descending coronary artery while a collateral flow limiting stenosis was present on the circumflex coronary artery. Epicardial BK was applied to small sponges (1 cm 2) which were placed on the anterior wall of the left ventricle. Intracoronary BK was injected into a branch of the anterior descending artery. We observed that mean maximal reflex increases in SNA during TMI and intracoronary BK were significantly greater in cardiac than in renal nerves (TMI; 58±11% versus 36±9%, p=0.01; intracoronary BK; 144±48% versus 77±26%, p=0.05). Epicardial BK elicited reflex increases in cardiac and renal SNA which were not significantly different (167±44% versus 127±36%; p=0.72). Our results indicate that activation of left ventricular sympathetic afferents by TMI and intracoronary BK elicits greater reflex increases in sympathetic outflow to the heart than to other end-organs such as the kidney. We speculate that these augmented excitatory responses are most likely related to engagement of cardio–cardiac spinal sympathetic reflexes during intense stimulation of sympathetic afferent endings.

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