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1 Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, Suita, Osaka, Japan; Japan Space Forum, Tokyo, Japan
2 Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, Suita, Osaka, Japan
3 Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, Suita, Osaka, Japan; The Organization for Pharmaceutical Safety and Research, Tokyo, Japan
* To whom correspondence should be addressed. E-mail: miyamoto{at}res.ncvc.go.jp.
To better understand the pathophysiological significance of high plasma norepinephrine (NE) concentration in regulating heart rate (HR), we examined the interactions between high plasma NE and the dynamic vagal control of HR. In anesthetized rabbits with sinoaortic denervation and vagotomy, we stimulated the right vagus using binary white noise sequence (0-10 Hz) for 10 min and estimated the transfer function from vagal stimulation to HR response. The transfer function approximated a first-order low-pass filter with pure delay. Intravenous infusion of NE (100 µg/kg/h) attenuated the dynamic gain from 6.2 ±0.8 to 3.9±1.2 beats/min/Hz (n=7, P<0.05) without affecting the corner frequency or pure delay. Simultaneous intravenous administration of phentolamine (1 mg/kg/h) and NE (100 µg/kg/h) abolished the inhibitory effect of NE on the dynamic gain (6.3±0.8 vs. 6.4±1.3 beats/min/Hz, NS, n=7). The inhibitory effect of NE on the dynamic vagal control of HR examined at infusion rates of 10, 50, and 100 µg/kg/h was dose-dependent (n=5). In conclusion, high plasma NE attenuated the dynamic HR response to vagal stimulation, probably via the activation of the 
-adrenergic receptors on the preganglionic and/or postganglionic cardiac vagal nerve terminals.
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