Basis for the preferential activation of cardiac sympathetic nerve activity in heart failure

R Ramchandra; SG Hood; DA Denton; RL Woods; MJ McKinley; RM McAllen; CN May

Journal article

Basis for the preferential activation of cardiac sympathetic nerve activity in heart failure

R Ramchandra, SG Hood, DA Denton, RL Woods, MJ McKinley, RM McAllen, CN May

Proceedings of the National Academy of Sciences of the United States of America | Published : 2009

DOI: 10.1073/pnas.0811929106

Abstract

In heart failure (HF) , sympathetic nerve activity is increased. Measurements in HF patients of cardiac norepinephrine spillover, reflecting cardiac sympathetic nerve activity (CSNA), indicate that it is increased earlier and to a greater extent than sympathetic activity to other organs. This has important consequences because it worsens prognosis, provoking arrhythmias and sudden death. To elucidate the mechanisms responsible for the activation of CSNA in HF, we made simultaneous direct neural recordings of CSNA and renal SNA (RSNA) in two groups of conscious sheep: normal animals and animals in HF induced by chronic, rapid ventricular pacing. In normal animals, the level of activity, measu..

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University of Melbourne Researchers

Clive May Author

Related Projects (5)

Cardiac Sympathetic Nerve Activity: understanding normal control and the causes of the increase in heart failure

Heart failure is a condition in which the heart muscle becomes weak and is unable to pump sufficient blood around the body to provide adequa..

Research Fellowship

Research Fellowship Renewal

Why is sympathetic nerve activity to the heart increased in heart failure?

Heart failure is a disabling and deadly syndrome that has reached epidemic proportions in western populations. In heart failure, the activit..

RESEARCH FELLOWSHIP 2007 - MCKINLEY

I am a neuroscientist-physiologist investigating the neural circuitry of body fluid homeostasis and autonomic function

Grants

Awarded by National Heart, Lung, and Blood Institute

Funding Acknowledgements

The authors thank Tony Dornom for technical assistance and David Trevaks for Spike 2 programming. This work was supported by National Health and Medical Research Council (NHMRC) of Australia Grants 232313 and 509204, National Heart Lung and Blood Institute Grant 5-R01-HL-07 4932, the Harold and Leila Mathers Charitable Trust, The Search Foundation, the Robert J. and Helen C. Klegberg Foundation, NHMRC Research Fellowships 350328 (to C.N.M.), 454369 (to M. J. M.), and 277901 (R. M. M.), and National Heart Foundation of Australia Postdoctoral Research Fellowship PF07M3293 (to R. R.).