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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.
Sundlöf et al. (1983) studied this question.