Tonic arterial chemoreceptor activity contributes to cardiac, but not renal, sympathetic activation in heart failure (1169.2)

Abstract

In heart failure (HF) cardiac sympathetic nerve activity (CSNA) is increased, which has detrimental effects on the heart. The arterial chemoreceptor activation plays an important role in stimulating renal SNA (RSNA) and muscle SNA in HF. We recorded CSNA and renal SNA (RSNA) in conscious normal sheep and in sheep with mild HF induced by rapid ventricular pacing (ejection fraction <40%). Tonic arterial chemoreceptor function was evaluated by deactivating chemoreceptors by supplementing room air with intranasal 100% oxygen (2‐3 L/min) for 20 min. In HF, chemoreceptor deactivation induced by hyperoxia reduced CSNA (90±2 vs. 75±5 bursts/100 beats, P<0.05; 86±5 vs. 66±7 bursts/min, P<0.001; n=10; hyperoxia vs. room air) and HR (96±4 vs 85±4 beats/min, P<0.001; n=12), but not RSNA burst incidence (93±4 vs 92±4 bursts/100beats; n=7), although due to the bradycardia RSNA burst frequency was decreased (90±8 vs 77±7 bursts/min; P<0.001). In normal sheep, chemoreceptor deactivation reduced HR without a significant effect on CSNA and RSNA. In HF, the response of CSNA, but not RSNA, to sodium cyanide injection was enhanced compared with normal sheep. There was no change in baroreflex control of HR, CSNA and RSNA either HF or normal sheep. In an ovine model of HF, tonic arterial chemoreceptor activation plays a critical role in stimulating the increased sympathetic activity to the heart.Grant Funding Source: Supported by NHMRC 628573, 07M 3293, 566819