QUANTITATIVE STUDY OF MUSCLE NERVE SYMPATHETIC ACTIVITY IN RESTING NORMOTENSIVE AND HYPERTENSIVE SUBJECTS

Recordings of multi-unit sympathetic activity were made from muscle branches of the peroneal or median nerves in 33 healthy and 12 hypertensive subjects resting in tbe recumbent position. Simultaneous recordings of intra-arterial blood pressure were made on 17 nonnotensive and all hypertensive subjects. The neural activity, quantified by counting the number of sympathetic pulse-synchronous impulse bursts in the mean voltage neurogram (burst incidence) was plotted against the age and the arterial blood pressure level of the subjects. Between different subjects there were marked differences in mean burst incidence, from less than 10 to more than 90 bursts/100 heart beats and there was a tendency for increasing values with increasing age. Taking the age differences into account there was no significant correlation between the amount of activity and the blood pressure level. The effect of spontaneous temporary blood pressure fluctuations was studied by correlating different pressure parameters of individual heart beats to the probability of occurrence of a sympathetic burst and to the mean voltage amplitude of the occurring burst. Irrespective of the mean burst incidence, the occurrence of the bursts and their mean voltage amplitudes were determined mainly by fluctuations of the diastollc blood pressure. The diastolic blood pressure threshold for sympathetic outflow was found to be reset to higher blood pressure values in the hypertensive subjects and the variability of their thresholds was also greater than for the normotensive controls. At a given diastolic blood pressure, more sympathetic activity occurred if diastolic blood pressure was falling than if it was rising, and this directional dependence was more pronounced in the hypertensive subjects. We suggest that the increased directional dependence accounts for the greater variability of the blood pressure threshold for sympathetic outflow in the hypertensive subjects. The differences can be explained on the basis of findings in animals with experimental hypertension, and it appears that they are secondary to the hypertension. © 1979 American Heart Association, Inc.