Sympathetic neural regulation of heart rate is robust against high plasma catecholamines

Toru Kawada, Tadayoshi Miyamoto, Yuichiro Miyoshi, Sayo Yamaguchi, Yukiko Tanabe, Atsunori Kamiya, Toshiaki Shishido, Masaru Sugimachi

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

The sympathetic regulation of heart rate (HR) may be attained by neural and humoral factors. With respect to the humoral factor, plasma noradrenaline (NA) and adrenaline (Adr) can reportedly increase to levels approximately 10 times higher than resting level during severe exercise. Whether such high plasma NA or Adr interfered with the sympathetic neural regulation of HR remained unknown. We estimated the transfer function from cardiac sympathetic nerve stimulation (SNS) to HR in anesthetized and vagotomized rabbits. An intravenous administration of NA (n = 6) at 1 and 10 μg·kg -1·h -1 increased plasma NA concentration (pg/ml) from a baseline level of 438 ± 117 (mean ± SE) to 974 ± 106 and 6,830 ± 917 (P < 0.01), respectively. The dynamic gain (bpm/Hz) of the transfer function did not change significantly (from 7.6 ± 1.2 to 7.5 ± 1.1 and 8.1 ± 1.1), whereas mean HR (in bpm) during SNS slightly increased from 280 ± 24 to 289 ± 22 (P < 0.01) and 288 ± 22 (P < 0.01). The intravenous administration of Adr (n = 6) at 1 and 10 μg·kg -1·h -1increased plasma Adr concentration (pg/ml) from a baseline level of 257 ± 86 to 659 ± 172 and 2,760 ± 590 (P < 0.01), respectively. Neither the dynamic gain (from 8.0 ± 0.6 to 8.4 ± 0.8 and 8.2 ± 1.0) nor the mean HR during SNS (from 274 ± 13 to 275 ±13 and 274 ± 13) changed significantly. In contrast, the intravenous administration of isoproterenol (n = 6) at 10 μg·kg -1·h -1significantly increased mean HR during SNS (from 278 ± 11 to 293 ± 9, P < 0.01) and blunted the transfer gain value at 0.0078 Hz (from 5.9 ± 1.0 to 1.0 ± 0.4, P < 0.01). In conclusion, high plasma NA or Adr hardly affected the dynamic sympathetic neural regulation of HR.

Original languageEnglish
Pages (from-to)235-245
Number of pages11
JournalJournal of Physiological Sciences
Volume56
Issue number3
DOIs
Publication statusPublished - Jun 1 2006
Externally publishedYes

Fingerprint

Catecholamines
Heart Rate
Epinephrine
Norepinephrine
Intravenous Administration
Isoproterenol
Rabbits

Keywords

  • Adrenaline
  • Isoproterenol
  • Neuro-humoral interaction
  • Noradrenaline
  • Systems analysis

ASJC Scopus subject areas

  • Physiology

Cite this

Sympathetic neural regulation of heart rate is robust against high plasma catecholamines. / Kawada, Toru; Miyamoto, Tadayoshi; Miyoshi, Yuichiro; Yamaguchi, Sayo; Tanabe, Yukiko; Kamiya, Atsunori; Shishido, Toshiaki; Sugimachi, Masaru.

In: Journal of Physiological Sciences, Vol. 56, No. 3, 01.06.2006, p. 235-245.

Research output: Contribution to journalArticle

Kawada, T, Miyamoto, T, Miyoshi, Y, Yamaguchi, S, Tanabe, Y, Kamiya, A, Shishido, T & Sugimachi, M 2006, 'Sympathetic neural regulation of heart rate is robust against high plasma catecholamines', Journal of Physiological Sciences, vol. 56, no. 3, pp. 235-245. https://doi.org/10.2170/physiolsci.RP006006
Kawada, Toru ; Miyamoto, Tadayoshi ; Miyoshi, Yuichiro ; Yamaguchi, Sayo ; Tanabe, Yukiko ; Kamiya, Atsunori ; Shishido, Toshiaki ; Sugimachi, Masaru. / Sympathetic neural regulation of heart rate is robust against high plasma catecholamines. In: Journal of Physiological Sciences. 2006 ; Vol. 56, No. 3. pp. 235-245.
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abstract = "The sympathetic regulation of heart rate (HR) may be attained by neural and humoral factors. With respect to the humoral factor, plasma noradrenaline (NA) and adrenaline (Adr) can reportedly increase to levels approximately 10 times higher than resting level during severe exercise. Whether such high plasma NA or Adr interfered with the sympathetic neural regulation of HR remained unknown. We estimated the transfer function from cardiac sympathetic nerve stimulation (SNS) to HR in anesthetized and vagotomized rabbits. An intravenous administration of NA (n = 6) at 1 and 10 μg·kg -1·h -1 increased plasma NA concentration (pg/ml) from a baseline level of 438 ± 117 (mean ± SE) to 974 ± 106 and 6,830 ± 917 (P < 0.01), respectively. The dynamic gain (bpm/Hz) of the transfer function did not change significantly (from 7.6 ± 1.2 to 7.5 ± 1.1 and 8.1 ± 1.1), whereas mean HR (in bpm) during SNS slightly increased from 280 ± 24 to 289 ± 22 (P < 0.01) and 288 ± 22 (P < 0.01). The intravenous administration of Adr (n = 6) at 1 and 10 μg·kg -1·h -1increased plasma Adr concentration (pg/ml) from a baseline level of 257 ± 86 to 659 ± 172 and 2,760 ± 590 (P < 0.01), respectively. Neither the dynamic gain (from 8.0 ± 0.6 to 8.4 ± 0.8 and 8.2 ± 1.0) nor the mean HR during SNS (from 274 ± 13 to 275 ±13 and 274 ± 13) changed significantly. In contrast, the intravenous administration of isoproterenol (n = 6) at 10 μg·kg -1·h -1significantly increased mean HR during SNS (from 278 ± 11 to 293 ± 9, P < 0.01) and blunted the transfer gain value at 0.0078 Hz (from 5.9 ± 1.0 to 1.0 ± 0.4, P < 0.01). In conclusion, high plasma NA or Adr hardly affected the dynamic sympathetic neural regulation of HR.",
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