Hypertension, Vol 5, 749-756, Copyright © 1983 by American Heart Association
G Sundlof, BG Wallin, E Stromgren and C Nerhed
Recordings of multiunit sympathetic activity were made from muscle branches
of the peroneal nerve in eight previously untreated subjects with essential
hypertension during intravenous administration of the cardioselective
beta-adrenoceptor antagonist, metoprolol. Intraarterial blood pressure and
central venous pressure were monitored simultaneously. After metoprolol,
heart rate fell and central venous pressure increased in all subjects.
Blood pressure increased in some subjects and decreased in others whereas
the rate of rise of the systolic pulse wave regularly decreased.
Sympathetic activity, discharged in pulse synchronous bursts of action
potentials, was quantitated by counting the number of bursts and their
amplitudes in the mean voltage neurogram. In all subjects, the average
diastole was associated with outflow of more sympathetic impulses after
metoprolol than before. Total sympathetic activity (expressed as bursts/min
multiplied by mean burst strength) also increased after the drug. The
mechanism behind the increase of sympathetic activity may be either a
direct central nervous effect or a reflex effect elicited from arterial
baroreceptors or cardiac receptors.
ARTICLES
Acute effects of metoprolol on muscle sympathetic activity in hypertensive humans
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