Tonic arterial chemoreceptor activity contributes to cardiac sympathetic activation in mild ovine heart failure. Issue 8 (14th July 2014)

• Record Type: Journal Article
• Authors: Xing, Daniel T.; May, Clive N.; Booth, Lindsea C.; Ramchandra, Rohit
• Is Part Of: Experimental physiology. Volume 99:Issue 8(2014:Aug.)
• Page Start: 1031
• Page End: 1041
• Publication Date: 2014-07-14
• Subjects: Physiology, Experimental -- Periodicals; 571.0724
• DOI: 10.1113/expphysiol.2014.079491
• Languages: English
• ISSNs: 0958-0670

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="eph1469-sec-0010" sec-type="section"> <title>New Findings</title> <p> <list id="eph1469-list-0001" list-type="bullet"> <list-item> <p> <bold>What is the central question of this study?</bold> </p> <p>What is the role of the peripheral chemoreflex in driving the increased levels of cardiac sympathetic nerve activity in heart failure?</p> </list-item> <list-item> <p> <bold>What is the main finding and its importance?</bold> </p> <p>We show that chemoreceptor deactivation by hyperoxia significantly decreased the elevated levels of cardiac sympathetic nerve activity and heart rate in mild ovine heart failure. Our findings suggest that interventional strategies that reduce chemoreceptor afferent activity in heart failure will reduce the elevated level of cardiac sympathetic drive and its associated detrimental effects.</p> </list-item> </list> </p> </sec> <sec id="eph1469-sec-0020" sec-type="section"> <p>Heart failure (HF) is associated with a large increase in cardiac sympathetic nerve activity (CSNA), which has detrimental effects on the heart and promotes arrhythmias and sudden death. There is increasing evidence that arterial chemoreceptor activation plays an important role in stimulating renal sympathetic nerve activity (RSNA) and muscle sympathetic nerve activity in HF. Given that sympathetic nerve activity to individual organs is differentially controlled, we investigated whether tonic arterial chemoreceptor activation contributes to the increased CSNA in HF. We recorded CSNA and 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 supplementing room air with 100% intranasal oxygen (2–3 l min<sup>−1</sup>) for 20 min, thereby deactivating chemoreceptors. The effects of hyperoxia on resting levels and baroreflex control of heart rate, CSNA and RSNA were determined. In HF, chemoreceptor deactivation induced by hyperoxia significantly reduced CSNA [90 ± 2 <italic>versus</italic> 75 ± 5 bursts (100 heart beats)<sup>−1</sup>, <italic>P</italic> < 0.05, <italic>n</italic> = 10; room air <italic>versus</italic> hyperoxia] and heart rate (96 ± 4 <italic>versus</italic> 85 ± 4 beats min<sup>−1</sup>, <italic>P</italic> < 0.001, <italic>n</italic> = 12). There was no change in RSNA burst incidence [93 ± 4 <italic>versus</italic> 92 ± 4 bursts (100 heart beats)<sup>−1</sup>, <italic>n</italic> = 7], although due to the bradycardia the RSNA burst frequency was decreased (90 ± 8 <italic>versus</italic> 77 ± 7 bursts min<sup>−1</sup>, <italic>P</italic> < 0.001). In normal sheep, chemoreceptor deactivation reduced heart rate without a significant effect on CSNA or RSNA. In summary, deactivation of peripheral chemoreceptors during HF reduced the elevated levels of CSNA, indicating that tonic arterial chemoreceptor activation plays a critical role in stimulating the elevated CSNA in HF.</p> </sec> </abstract>