Acute β-blockade increases muscle sympathetic activity and modifies its frequency distribution

Chiara Cogliati, Simona Colombo, Tomaso Gnecchi Ruscone, Domenico Gruosso, Alberto Porta, Nicola Montano, Alberto Malliani, Raffaello Furlan

Research output: Contribution to journalArticle

Abstract

Background - The possible mechanisms by which β-adrenergic antagonists may act on the neural regulation of the cardiovascular system are still elusive. Recent studies reported a marked increase of postganglionic muscle sympathetic nerve activity (MSNA) after acute β-blockade associated with unchanged values of arterial blood pressure and baroreflex sensitivity. We tested the hypothesis that acute β-blockade might also alter the oscillatory characteristics of MSNA, thus decreasing its effectiveness on peripheral vasoconstriction. Methods and Results - In 11 healthy volunteers, ECG, MSNA, arterial pressure, and respiration were recorded before and after atenolol (0.05 mg/kg IV bolus) administration. The frequency distribution of RR interval, MSNA, systolic arterial pressure (SAP), and respiratory variability was assessed by spectrum and cross-spectrum analysis. Spontaneous baroreflex sensitivity (α-index) and plasma catecholamines (high-performance liquid chromatography) were measured. Atenolol induced a significant increase in RR interval (14.3±1.6%) with no changes in systolic and diastolic arterial pressure. MSNA increased (42±13% from 18±2 bursts per minute). The low-frequency (LF) component of RR and MSNA variability decreased (-44±7% and -24±5%, respectively), whereas the high-frequency (HF) component increased (163±55% and 34±11%, respectively), expressed in normalized units. Spectral coherence, an index of oscillatory coupling, decreased between LFRR and LFMSNA, whereas it increased between HFMSNA and HFResp. SAP variability, α-index, and plasma catecholamines remained unchanged. Conclusions - Atenolol induced a change in MSNA frequency distribution reflecting a stronger respiratory coupling. This shift toward high frequency, despite an increase in MSNA, may lead to a less efficient sympathetic vasomotor modulation.

Original languageEnglish
Pages (from-to)2786-2791
Number of pages6
JournalCirculation
Volume110
Issue number18
DOIs
Publication statusPublished - Nov 2 2004

Fingerprint

Muscles
Arterial Pressure
Atenolol
Baroreflex
Blood Pressure
Catecholamines
Adrenergic Antagonists
Cardiovascular System
Vasoconstriction
Spectrum Analysis
Healthy Volunteers
Electrocardiography
Respiration
High Pressure Liquid Chromatography

Keywords

  • Adrenergic β-antagonists
  • Baroreceptors
  • Nervous system, autonomic
  • Nervous system, sympathetic

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Acute β-blockade increases muscle sympathetic activity and modifies its frequency distribution. / Cogliati, Chiara; Colombo, Simona; Ruscone, Tomaso Gnecchi; Gruosso, Domenico; Porta, Alberto; Montano, Nicola; Malliani, Alberto; Furlan, Raffaello.

In: Circulation, Vol. 110, No. 18, 02.11.2004, p. 2786-2791.

Research output: Contribution to journalArticle

Cogliati, Chiara ; Colombo, Simona ; Ruscone, Tomaso Gnecchi ; Gruosso, Domenico ; Porta, Alberto ; Montano, Nicola ; Malliani, Alberto ; Furlan, Raffaello. / Acute β-blockade increases muscle sympathetic activity and modifies its frequency distribution. In: Circulation. 2004 ; Vol. 110, No. 18. pp. 2786-2791.
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T1 - Acute β-blockade increases muscle sympathetic activity and modifies its frequency distribution

AU - Cogliati, Chiara

AU - Colombo, Simona

AU - Ruscone, Tomaso Gnecchi

AU - Gruosso, Domenico

AU - Porta, Alberto

AU - Montano, Nicola

AU - Malliani, Alberto

AU - Furlan, Raffaello

PY - 2004/11/2

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AB - Background - The possible mechanisms by which β-adrenergic antagonists may act on the neural regulation of the cardiovascular system are still elusive. Recent studies reported a marked increase of postganglionic muscle sympathetic nerve activity (MSNA) after acute β-blockade associated with unchanged values of arterial blood pressure and baroreflex sensitivity. We tested the hypothesis that acute β-blockade might also alter the oscillatory characteristics of MSNA, thus decreasing its effectiveness on peripheral vasoconstriction. Methods and Results - In 11 healthy volunteers, ECG, MSNA, arterial pressure, and respiration were recorded before and after atenolol (0.05 mg/kg IV bolus) administration. The frequency distribution of RR interval, MSNA, systolic arterial pressure (SAP), and respiratory variability was assessed by spectrum and cross-spectrum analysis. Spontaneous baroreflex sensitivity (α-index) and plasma catecholamines (high-performance liquid chromatography) were measured. Atenolol induced a significant increase in RR interval (14.3±1.6%) with no changes in systolic and diastolic arterial pressure. MSNA increased (42±13% from 18±2 bursts per minute). The low-frequency (LF) component of RR and MSNA variability decreased (-44±7% and -24±5%, respectively), whereas the high-frequency (HF) component increased (163±55% and 34±11%, respectively), expressed in normalized units. Spectral coherence, an index of oscillatory coupling, decreased between LFRR and LFMSNA, whereas it increased between HFMSNA and HFResp. SAP variability, α-index, and plasma catecholamines remained unchanged. Conclusions - Atenolol induced a change in MSNA frequency distribution reflecting a stronger respiratory coupling. This shift toward high frequency, despite an increase in MSNA, may lead to a less efficient sympathetic vasomotor modulation.

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