title: Acute beta-blockade increases muscle sympathetic activity and modifies its frequency distribution.
abstract: BACKGROUND
  The possible mechanisms by which beta-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 beta-blockade associated with unchanged values of arterial blood pressure and baroreflex sensitivity. We tested the hypothesis that acute beta-blockade might also alter the oscillatory characteristics of MSNA, thus decreasing its effectiveness on peripheral vasoconstriction.
  
  
  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 LF(RR) and LF(MSNA), whereas it increased between HF(MSNA) and HF(Resp). 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.
authors.affiliation: Medicina Interna II, Ospedale L. Sacco, Milano, Italy.
authors.forename: Chiara
authors.initials: C
authors.lastname: Cogliati
authors.forename: Simona
authors.initials: S
authors.lastname: Colombo
authors.forename: Tomaso Gnecchi
authors.initials: TG
authors.lastname: Ruscone
authors.forename: Domenico
authors.initials: D
authors.lastname: Gruosso
authors.forename: Alberto
authors.initials: A
authors.lastname: Porta
authors.forename: Nicola
authors.initials: N
authors.lastname: Montano
authors.forename: Alberto
authors.initials: A
authors.lastname: Malliani
authors.forename: Raffaello
authors.initials: R
authors.lastname: Furlan
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000319:Adrenergic beta-Antagonists / Q000008:administration & dosage / Q000494:pharmacology*; D000328:Adult; D001262:Atenolol / Q000008:administration & dosage / Q000494:pharmacology*; D017704:Baroreflex / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects; D004562:Electrocardiography; D004837:Epinephrine / Q000097:blood; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D007275:Injections, Intravenous; D008297:Male; D018482:Muscle, Skeletal / Q000294:innervation*; D009638:Norepinephrine / Q000097:blood; D010543:Peroneal Nerve / Q000187:drug effects* / Q000502:physiology; D012119:Respiration / Q000187:drug effects; D017779:Sympathetic Fibers, Postganglionic / Q000187:drug effects* / Q000502:physiology; D014661:Vasoconstriction / Q000187:drug effects; D014666:Vasomotor System / Q000187:drug effects
chemical_list: D000319:Adrenergic beta-Antagonists; D001262:Atenolol; D009638:Norepinephrine; D004837:Epinephrine