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Circulation. 2004;110:2786-2791
Published online before print October 25, 2004, doi: 10.1161/01.CIR.0000146335.69413.F9
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(Circulation. 2004;110:2786-2791.)
© 2004 American Heart Association, Inc.


Arrhythmia/Electrophysiology

Acute ß-Blockade Increases Muscle Sympathetic Activity and Modifies Its Frequency Distribution

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

From Medicina Interna II, Ospedale L. Sacco, Milano (C.C., N.M., A.M., R.F.); Dipartimento Scienze Precliniche LITA di Vialba (A.P.); Università degli Studi di Milano, Divisioni di Cardiologia, Ospedali di Rho (S.C.) e Merate (T.G.R.), Milano; and Medicina Interna, Università Seconda, Napoli (D.G.), Italy.

Correspondence to Dr Raffaello Furlan, Unità Sincopi e Disturbi della Postura, Medicina Interna II, Ospedale L. Sacco, Università di Milano, Via G.B. Grassi 74, 20157 Milano, Italy. E-mail raffaellof{at}fisiopat.sacco.unimi.it

Received February 27, 2003; de novo received December 16, 2003; revision received March 30, 2004; accepted April 2, 2004.

Background— The possible mechanisms by which ß-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 ß-blockade associated with unchanged values of arterial blood pressure and baroreflex sensitivity. We tested the hypothesis that acute ß-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 ({alpha}-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, {alpha}-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.


Key Words: adrenergic ß-antagonists • nervous system, sympathetic • nervous system, autonomic • baroreceptors


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