Resting Levels and Baroreflex Control of Cardiac and Renal Sympathetic Nerve Activity in Heart Failure

Abstract

During heart failure (HF), cardiac noradrenaline release is increased by up to 50‐fold, a much greater increase than from other organs. The reasons behind this preferential activation of cardiac sympathetic nerve activity (SNA) remain unclear. We hypothesised that the basal level of cardiac SNA in normal animals is set at a lower percentage of its maximum than is SNA to other organs. To investigate this possibility we measured cardiac SNA and renal SNA simultaneously in conscious sheep, at least 4 days after surgery. Experiments were conducted in normal (n = 7) and HF animals (n = 7). Consistent with our hypothesis, the burst frequency of cardiac SNA was significantly lower than renal SNA in normal animals (35 ± 7 % cardiac vs. 92 ± 2 % renal; P<0.05). Furthermore, the resting level of cardiac SNA was set at a lower percentage of maximum compared to renal SNA. HF was associated with an increase in the baseline activity of both nerves to similar levels compared to their maximum. HF was not accompanied by a change in baroreflex gain of either cardiac or renal SNA compared to normal animals. Our results indicate that in the normal state the resting level of cardiac SNA is set lower than renal SNA and during HF the SNA to both organs are increased to similar levels of maximum. This result offers one explanation for the preferential increase in cardiac noradrenaline spillover observed in HF. Funded by NHMRC, Australia and NIH.