Bidirectional augmentation of heart rate regulation by autonomic nervous system in rabbits.

Although the characteristics of the static interaction between the sympathetic and parasympathetic nervous systems in regulating heart rate (HR) have been well established, how the dynamic interaction modulates the HR response remains unknown. We therefore investigated dynamic interaction by estimating the transfer function from nerve stimulation to HR using a band-limited Gaussian white-noise technique. The transfer function relating dynamic sympathetic stimulation to HR had characteristics of a second-order low-pass filter. Simultaneous tonic vagal stimulation at 5 and 10 Hz increased gain of the transfer function by 55.0 +/- 40.1 and 80.7 +/- 50.5%, respectively (P < 0.05). The transfer function from dynamic vagal stimulation to HR had characteristics of a first-order low-pass filter. Simultaneous tonic sympathetic stimulation at 5 and 10 Hz increased the gain by 18.2 +/- 17.9 and 24.1 +/- 18.0%, respectively (P < 0.05). Thus interaction augmented dynamic gain bidirectionally, even though it affected mean HR antagonistically. By virtue of this interaction, the autonomic nervous system appears to extend its dynamic range of operation.

[1]  M N Levy,et al.  Antecedent sympathetic stimulation alters time course of chronotropic response to vagal stimulation in dogs. , 1994, The American journal of physiology.

[2]  G. Glick,et al.  Relative Roles of the Sympathetic and Parasympathetic Nervous Systems in the Reflex Control of Heart Rate , 1965, Circulation research.

[3]  M. N. Levy Brief Reviews: Sympathetic-Parasympathetic Interactions in the Heart , 1971, Circulation research.

[4]  E. Braunwald,et al.  Neurotransmitter Control of Sinoatrial Pacemaker Frequency in Isolated Rat Atria and in Intact Rabbits , 1970, Circulation research.

[5]  K. Sunagawa,et al.  Arterial baroreflex dynamics in normotensive and spontaneously hypertensive rats. , 1992, The American journal of physiology.

[6]  D. McCloskey,et al.  Vagal stimulation and cardiac slowing. , 1984, Journal of the autonomic nervous system.

[7]  D. McCloskey,et al.  Sympathetic‐parasympathetic interactions at the heart, possibly involving neuropeptide Y, in anaesthetized dogs. , 1990, The Journal of physiology.

[8]  H. Winkler,et al.  Adrenergic mechanisms in the sinus node. , 1970, Archives of internal medicine.

[9]  M. N. Levy,et al.  Paradoxical effect of vagus nerve stimulation on heart rate in dogs. , 1969, Circulation research.

[10]  R. Russell,et al.  Effect of Combined Sympathetic and Vagal Stimulation on Heart Rate in the Dog , 1969, Circulation research.

[11]  M. N. Levy,et al.  Effect of Vagal Stimulation on the Overflow of Norepinephrine into the Coronary Sinus during Cardiac Sympathetic Nerve Stimulation in the Dog , 1976, Circulation research.

[12]  M. Sugimachi,et al.  Dynamic effects of carotid sinus baroreflex on ventriculoarterial coupling studied in anesthetized dogs. , 1992, Circulation research.

[13]  M. N. Levy,et al.  Sympathetic stimulation-evoked overflow of norepinephrine and neuropeptide Y from the heart. , 1991, Circulation research.

[14]  H. Warner,et al.  A mathematical model of heart rate control by sympathetic and vagus efferent information , 1962 .

[15]  A. Kadish,et al.  Dissociation of heart rate variability from parasympathetic tone. , 1994, The American journal of physiology.

[16]  K. Sunagawa,et al.  Role of carotid sinus baroreflex in attenuating systemic arterial pressure variability studied in anesthetized dogs. , 1994, The American journal of physiology.