Cited by 86Blood Pressure and Hypertension StudiesHeart Rate Variability and Autonomic ControlCardiovascular and exercise physiology

Sympathetic outflow to muscles during treatment of hypertension with metoprolol

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Wallin, B G, Sundlöf, G, Strömgren, E, Aberg, H·1984·Hypertension

Abstract

Microelectrode recordings of multiunit sympathetic vasoconstrictor activity were made in muscle branches of the peroneal nerve in patients with essential hypertension before and during long-term treatment with the cardioselective beta-adrenergic receptor antagonist metoprolol. Nerve activity was quantified by counting the number of sympathetic bursts in the mean voltage neurogram. Metoprolol treatment lowered blood pressure and heart rate in all subjects. During long-term treatment, nerve activity was reduced both when compared to the level of activity after the first dose of the drug (p less than 0.01) and when compared to the control level before treatment (p less than 0.05). It is suggested that the reduction of sympathetic vasoconstrictor outflow to muscles contributed to the blood pressure reduction.

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Crossref · 10.1161/01.hyp.6.4.557

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  • The increased sympathetic activity in EHT+LVH was not attributable to antihypertensive treatment.

    “Therefore, the increased activity in EHT + LVH was not attributable to antihypertensive treatment and, in fact, was still apparent despite the use of agents”
  • Chronic administration of atenolol or metoprolol may have either no effect on or reduce the resting mean frequency of sympathetic discharge in essential hypertension.

    “However, chronic administration, as in this study, with agents such as atenolol (29)and metoprolol (30)may, respectively, have either no effect on or reduce the resting mean frequency of sympathetic discharge in EHT.”
  • Although an effect of medications in the two hypertensive groups cannot be completely excluded, they could not have entirely caused the excessive sympathetic hyperactivity.

    “Therefore, although we cannot completely exclude an effect of medications in our 2 hypertensive groups, they could not have entirely caused the excessive sympathetic hyperactivity.”
  • β-blockers may have no effect or decrease MSNA in hypertensive patients.

    “Although we cannot entirely exclude some influence of these agents, it is known in hypertensive patients that chronic ACE inhibitor therapy does not affect MSNA levels, 22 ARBs may decrease it, 23 and ␤-blockers may have no effect or decrease MSNA.24,25”

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References 18 · Cited by 86

Authors
Wallin, B. G., Sundlöf, G., Strömgren, E., & Aberg, H.
Venue
Hypertension
Published
1984-07
Volume
6
Issue
4
Pages
557-562
ISSN
  • 0194-911X (ISSN-L)
  • 1524-4563
OpenAlex
W2076073800
Cited by
86
References
18
Citations by year
2025: 2 · 2021: 1 · 2019: 1 · 2018: 1 · 2016: 2 · 2015: 1 · 2014: 1 · 2013: 3 · 2012: 2
FWCI
2.38
Type
journal article
Language
en
Open access
Locations
  • Hypertension (publishedVersion)
  • PubMed (publishedVersion)
Funders
Medical Research Council
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Rate Variability and Autonomic Control
  • Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
Keywords
metoprolol, essential hypertension, peroneal nerve, beta-blockers, blood pressure reduction, heart rate reduction, microelectrode recording
MeSH terms
Adult, Blood Pressure, Female, Heart Rate, Humans, Hypertension, Male, Metoprolol, Microelectrodes, Middle Aged, Muscles, Norepinephrine, Renin, Sympathetic Nervous System

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