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NEUROHUMORAL CONTROL OF CIRCULATION AND HYPERTENSION

Intrinsic cardiac nervous system in tachycardia induced heart failure

¹Department of Anatomy, Neurobiology, and Surgery, Dalhousie University, Halifax, Nova Scotia B3H 4B7; ²Department of Pharmacology, University of Montréal, Montréal, Québec, Canada H4J 1C5; ³Department of Pharmacology, East Tennessee State University, Johnson City, Tennessee 37614; and ⁴Department of Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, Alabama 35294-0005

Submitted 11 March 2003 ; accepted in final form 15 July 2003

The purpose of this study was to test the hypothesis that early-stage heart failure differentially affects the intrinsic cardiac nervous system's capacity to regulate cardiac function. After 2 wk of rapid ventricular pacing in nine anesthetized canines, cardiac and right atrial neuronal function were evaluated in situ in response to enhanced cardiac sensory inputs, stimulation of extracardiac autonomic efferent neuronal inputs, and close coronary arterial administration of neurochemicals that included nicotine. Right atrial neuronal intracellular electrophysiological properties were then evaluated in vitro in response to synaptic activation and nicotine. Intrinsic cardiac nicotine-sensitive, neuronally induced cardiac responses were also evaluated in eight sham-operated, unpaced animals. Two weeks of rapid ventricular pacing reduced the cardiac index by 54%. Intrinsic cardiac neurons of paced hearts maintained their cardiac mechano- and chemosensory transduction properties in vivo. They also responded normally to sympathetic and parasympathetic preganglionic efferent neuronal inputs, as well as to locally administered -or -adrenergic agonists or angiotensin II. The dose of nicotine needed to modify intrinsic cardiac neurons was 50 times greater in failure compared with normal preparations. That dose failed to alter monitored cardiovascular indexes in failing preparations. Phasic and accommodating neurons identified in vitro displayed altered intracellular membrane properties compared with control, including decreased membrane resistance, indicative of reduced excitability. Early-stage heart failure differentially affects the intrinsic cardiac nervous system's capacity to regulate cardiodynamics. While maintaining its capacity to transduce cardiac mechano- and chemosensory inputs, as well as inputs from extracardiac autonomic efferent neurons, intrinsic cardiac nicotine-sensitive, local-circuit neurons differentially remodel such that their capacity to influence cardiodynamics becomes obtunded.

pacing-induced heart failure; intrinsic cardiac neurons; atrial neuron; nicotinic receptors; parasympathetic efferent neurons; sympathetic efferent neurons

This article has been cited by other articles:

				M. Waldmann, G. W. Thompson, G. C. Kember, J. L. Ardell, and J. A. Armour Stochastic behavior of atrial and ventricular intrinsic cardiac neurons J Appl Physiol, August 1, 2006; 101(2): 413 - 419. [Abstract] [Full Text] [PDF]

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