Angiotensin II disproportionally attenuates dynamic vagal and sympathetic heart rate controls

Toru Kawada, Masaki Mizuno, Shuji Shimizu, Kazunori Uemura, Atsunori Kamiya, Masaru Sugimachi

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

To better understand the pathophysiological role of angiotensin II (ANG II) in the dynamic autonomic regulation of heart rate (HR), we examined the effects of intravenous administration of ANG II (10 μg·kg -1·h-1) on the transfer function from vagal or sympathetic nerve stimulation to HR in anesthetized rabbits with sinoaortic denervation and vagotomy. In the vagal stimulation group (n = 7), we stimulated the right vagal nerve for 10 min using binary white noise (0-10 Hz). The transfer function from vagal stimulation to HR approximated a first-order low-pass filter with pure delay. ANG II attenuated the dynamic gain from 7.6 ± 0.9 to 5.8 ± 0.9 beats·min-1·Hz -1 (means ± SD; P < 0.01) without affecting the corner frequency or pure delay. In the sympathetic stimulation group (n = 7), we stimulated the right postganglionic cardiac sympathetic nerve for 20 min using binary white noise (0-5 Hz). The transfer function from sympathetic stimulation to HR approximated a second-order low-pass filter with pure delay. ANG II slightly attenuated the dynamic gain from 10.8 ± 2.6 to 10.2 ± 3.1 beats·min-1·Hz-1 (P = 0.049) without affecting the natural frequency, damping ratio, or pure delay. The disproportional suppression of the dynamic vagal and sympathetic regulation of HR would result in a relative sympathetic predominance in the presence of ANG II. The reduced high-frequency component of HR variability in patients with cardiovascular diseases, such as myocardial infarction and heart failure, may be explained in part by the peripheral effects of ANG II on the dynamic autonomic regulation of HR.

Original languageEnglish
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume296
Issue number5
DOIs
Publication statusPublished - May 1 2009
Externally publishedYes

Fingerprint

Angiotensin II
Heart Rate
Heart Failure
Vagotomy
Denervation
Intravenous Administration
Cardiovascular Diseases
Myocardial Infarction
Rabbits

Keywords

  • Cardiac sympathetic nerve activity
  • Heart rate variability
  • Rabbit
  • Systems analysis
  • Transfer function

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)
  • Cardiology and Cardiovascular Medicine

Cite this

Angiotensin II disproportionally attenuates dynamic vagal and sympathetic heart rate controls. / Kawada, Toru; Mizuno, Masaki; Shimizu, Shuji; Uemura, Kazunori; Kamiya, Atsunori; Sugimachi, Masaru.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 296, No. 5, 01.05.2009.

Research output: Contribution to journalArticle

Kawada, Toru ; Mizuno, Masaki ; Shimizu, Shuji ; Uemura, Kazunori ; Kamiya, Atsunori ; Sugimachi, Masaru. / Angiotensin II disproportionally attenuates dynamic vagal and sympathetic heart rate controls. In: American Journal of Physiology - Heart and Circulatory Physiology. 2009 ; Vol. 296, No. 5.
@article{ee1d8a6ed7144e22ae39d1d8a3c00e78,
title = "Angiotensin II disproportionally attenuates dynamic vagal and sympathetic heart rate controls",
abstract = "To better understand the pathophysiological role of angiotensin II (ANG II) in the dynamic autonomic regulation of heart rate (HR), we examined the effects of intravenous administration of ANG II (10 μg·kg -1·h-1) on the transfer function from vagal or sympathetic nerve stimulation to HR in anesthetized rabbits with sinoaortic denervation and vagotomy. In the vagal stimulation group (n = 7), we stimulated the right vagal nerve for 10 min using binary white noise (0-10 Hz). The transfer function from vagal stimulation to HR approximated a first-order low-pass filter with pure delay. ANG II attenuated the dynamic gain from 7.6 ± 0.9 to 5.8 ± 0.9 beats·min-1·Hz -1 (means ± SD; P < 0.01) without affecting the corner frequency or pure delay. In the sympathetic stimulation group (n = 7), we stimulated the right postganglionic cardiac sympathetic nerve for 20 min using binary white noise (0-5 Hz). The transfer function from sympathetic stimulation to HR approximated a second-order low-pass filter with pure delay. ANG II slightly attenuated the dynamic gain from 10.8 ± 2.6 to 10.2 ± 3.1 beats·min-1·Hz-1 (P = 0.049) without affecting the natural frequency, damping ratio, or pure delay. The disproportional suppression of the dynamic vagal and sympathetic regulation of HR would result in a relative sympathetic predominance in the presence of ANG II. The reduced high-frequency component of HR variability in patients with cardiovascular diseases, such as myocardial infarction and heart failure, may be explained in part by the peripheral effects of ANG II on the dynamic autonomic regulation of HR.",
keywords = "Cardiac sympathetic nerve activity, Heart rate variability, Rabbit, Systems analysis, Transfer function",
author = "Toru Kawada and Masaki Mizuno and Shuji Shimizu and Kazunori Uemura and Atsunori Kamiya and Masaru Sugimachi",
year = "2009",
month = "5",
day = "1",
doi = "10.1152/ajpheart.01041.2008",
language = "English",
volume = "296",
journal = "American Journal of Physiology",
issn = "0002-9513",
publisher = "American Physiological Society",
number = "5",

}

TY - JOUR

T1 - Angiotensin II disproportionally attenuates dynamic vagal and sympathetic heart rate controls

AU - Kawada, Toru

AU - Mizuno, Masaki

AU - Shimizu, Shuji

AU - Uemura, Kazunori

AU - Kamiya, Atsunori

AU - Sugimachi, Masaru

PY - 2009/5/1

Y1 - 2009/5/1

N2 - To better understand the pathophysiological role of angiotensin II (ANG II) in the dynamic autonomic regulation of heart rate (HR), we examined the effects of intravenous administration of ANG II (10 μg·kg -1·h-1) on the transfer function from vagal or sympathetic nerve stimulation to HR in anesthetized rabbits with sinoaortic denervation and vagotomy. In the vagal stimulation group (n = 7), we stimulated the right vagal nerve for 10 min using binary white noise (0-10 Hz). The transfer function from vagal stimulation to HR approximated a first-order low-pass filter with pure delay. ANG II attenuated the dynamic gain from 7.6 ± 0.9 to 5.8 ± 0.9 beats·min-1·Hz -1 (means ± SD; P < 0.01) without affecting the corner frequency or pure delay. In the sympathetic stimulation group (n = 7), we stimulated the right postganglionic cardiac sympathetic nerve for 20 min using binary white noise (0-5 Hz). The transfer function from sympathetic stimulation to HR approximated a second-order low-pass filter with pure delay. ANG II slightly attenuated the dynamic gain from 10.8 ± 2.6 to 10.2 ± 3.1 beats·min-1·Hz-1 (P = 0.049) without affecting the natural frequency, damping ratio, or pure delay. The disproportional suppression of the dynamic vagal and sympathetic regulation of HR would result in a relative sympathetic predominance in the presence of ANG II. The reduced high-frequency component of HR variability in patients with cardiovascular diseases, such as myocardial infarction and heart failure, may be explained in part by the peripheral effects of ANG II on the dynamic autonomic regulation of HR.

AB - To better understand the pathophysiological role of angiotensin II (ANG II) in the dynamic autonomic regulation of heart rate (HR), we examined the effects of intravenous administration of ANG II (10 μg·kg -1·h-1) on the transfer function from vagal or sympathetic nerve stimulation to HR in anesthetized rabbits with sinoaortic denervation and vagotomy. In the vagal stimulation group (n = 7), we stimulated the right vagal nerve for 10 min using binary white noise (0-10 Hz). The transfer function from vagal stimulation to HR approximated a first-order low-pass filter with pure delay. ANG II attenuated the dynamic gain from 7.6 ± 0.9 to 5.8 ± 0.9 beats·min-1·Hz -1 (means ± SD; P < 0.01) without affecting the corner frequency or pure delay. In the sympathetic stimulation group (n = 7), we stimulated the right postganglionic cardiac sympathetic nerve for 20 min using binary white noise (0-5 Hz). The transfer function from sympathetic stimulation to HR approximated a second-order low-pass filter with pure delay. ANG II slightly attenuated the dynamic gain from 10.8 ± 2.6 to 10.2 ± 3.1 beats·min-1·Hz-1 (P = 0.049) without affecting the natural frequency, damping ratio, or pure delay. The disproportional suppression of the dynamic vagal and sympathetic regulation of HR would result in a relative sympathetic predominance in the presence of ANG II. The reduced high-frequency component of HR variability in patients with cardiovascular diseases, such as myocardial infarction and heart failure, may be explained in part by the peripheral effects of ANG II on the dynamic autonomic regulation of HR.

KW - Cardiac sympathetic nerve activity

KW - Heart rate variability

KW - Rabbit

KW - Systems analysis

KW - Transfer function

UR - http://www.scopus.com/inward/record.url?scp=66149099167&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=66149099167&partnerID=8YFLogxK

U2 - 10.1152/ajpheart.01041.2008

DO - 10.1152/ajpheart.01041.2008

M3 - Article

C2 - 19252092

AN - SCOPUS:66149099167

VL - 296

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0002-9513

IS - 5

ER -