Clinical Science and Molecular Medicine (1973) 45, 127s-I 30s.
SYMPATHETIC ACTIVITY I N PERIPHERAL NERVES
O F NORMO- A N D HYPERTENSIVE SUBJECTS
B . G. W A L L I N , W. D E L I U S A N D K.-E. H A G B A R T H
Departments of Clinical Neurophysiology and Internal Medicine,
University Hospital, Uppsala, Sweden
SUMMARY
I . In hypertensive patients the general pattern of spontaneously occurring sympathetic activity (SA) as well as the sympathetic responses to various manoeuvres are
similar to those of the normotensive controls.
2. This suggests that the multi-unit SA recorded in muscle and skin nerves of hypertensive patients are made up of impulses from the same fibre populations as in
normotensive subjects and that the outflow of these impulses is controlled by similar
mechanisms in the two groups.
3. More quantitative evidence obtained under standardized external conditions is
necessary before it can be decided whether there is an increased strength of the
sympathetic outflow to the skin in hypertensive patients.
Key words : sympathetic nerve recordings, hypertension, man, muscle nerves, skin
nerves.
With the introduction of the microneurographic technique (Vallbo & Hagbarth, 1968) it
became possible to make direct recordings of sympathetic activity (SA) in the peripheral
nerves of unanaesthetized human beings and recently we described the characteristics of the
sympathetic outflow in skin and muscle nerves of healthy normotensive subjects (Delius,
Hagbarth, Hongell & Wallin, 1972a, b, c; Hagbarth, Hallin, Hongell, Torebjork & Wallin,
1972). In the present report these results will be compared with similar data obtained from
recordings of SA in patients with arterial hypertension.
MATERIAL AND METHODS
The comparison is based on recordings in twenty-four normotensive subjects (twelve men and
Correspondence: Dr B. G . Wallin, Department of Clinical Neurophysiology, University Hospital, 750 14
Uppsala 14, Sweden.
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B. G. Wallin, W. Delius and K.-E. Hagbarth
twelve women, 24-54 years old) and twenty-one hypertensive patients (eleven men and ten
women, 25-63 years old). After a thorough clinical investigation, in most cases including renal
arteriography, nineteen were considered to have ‘essential hypertension’; in the two remaining
cases secondary hypertension could not be excluded. Most of the hypertensive patients were
classified as WHO stage I and all had been without antihypertensive drugs at least 2 weeks
before the investigation.
Usually the nerve recordings were made in the peroneal or median nerve. The recording
technique, the procedure used for identifying pure muscle and skin nerve fascicles and the
methods of distinguishing between SA and other types of neural activity were the same as
described for the normotensive subjects (Delius et al., 1972a, b).
RESULTS
Muscle and skin nerve SA in normotensilve subjects
Recordings of SA in normotensive subjects showed that both the resting sympathetic
rhythms and the sympathetic responses to various manoeuvres were quite different in muscle
and skin nerve fascicles. I n muscle nerve fascicles the sympathetic impulses were grouped in
rather distinct pulse synchronous bursts occurring in more or less irregular sequences separated
by periods of neural silence. In skin nerve fascicles, on the other hand, the impulses occurred in
much more irregular bursts of varying duration showing no sign of pulse synchrony. Manoeuvres
giving rise to an increased SA in muscle nerves were regularly accompanied by plethysmographic signs of muscular vasoconstriction suggesting that the muscle nerve SA was dominated
by vasoconstrictor impulses. The skin nerve SA seemed to contain a mixture of vasoconstrictor
and sudomotor impulses since the sympathetic bursts in skin nerves were followed by plethysmographic signs of skin vasoconstriction and/or reductions of skin electrical resistance. The
difference in pattern of the SA in the two nerve types was thought to arise because the sympathetic outflow in muscle nerves is under strong baroreflex control whereas this does not seem
to be the case for the skin nerve SA. In accordance with this no correlation was seen between
skin nerve SA and blood pressure variations at rest whereas in the muscle nerves the pulse
synchronous burst sequencies regularly occurred during periods of reduced blood pressure
when each diastole caused a temporary reduction of baroreflex inhibition so that an efferent
volley of sympathetic impulses could be released. The periods of neural silence between the
burst sequences in muscle nerves corresponded to transient blood pressure increases when the
baroreflex inhibition of the vasomotor centres became strong enough completely to suppress
the outflow of sympathetic impulses. These inhibitions seemed to occur when the blood pressure exceeded a certain level which varied from subject to subject but usually was in the range
of 120-1 50/70-90mmHg. In muscle nerve recordings from the peroneal nerve at the knee level
the neural events succeeded the blood pressure changes with a delay of about 1.2 s.
Several procedures, such as Valsalva’s manoeuvre, muscle work, mental stress, temperature
changes, etc., were associated with changes of the sympathetic outflow which as a rule were
different in skin and muscle nerves. I n muscle nerves (during, e.g., Valsalva’s manoeuvre or
muscle work) the sympathetic responses reflected the homeostatic control function of the
skeletal muscle vascular bed and in skin nerves the changes of SA were brought about either in
situations related to the thermoregulatory function of the skin or during circulatory adjustments to different mental or emotional states.
Sympathetic activity in hypertensive patients
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Muscle nerve SA in hypertensive patients
When recording from muscle nerve fascicles in hypertensive patients at rest the sympathetic
impulses appeared in similar sequencies of pulse synchronous bursts as in normal subjects and
it was impossible to decide from the nerve record whether the patient was hypertensive or not.
As in the normal subjects the sympathetic bursts occurred during temporary blood pressure
reductions whereas transient blood pressure increases inhibited the sympathetic outflow. The
blood pressure level where a complete suppression of the SA occurred was around 150-200/
100-120 mmHg in the hypertensive patients which was higher than in the normotensive group.
This upward shift of the inhibitory blood pressure level agrees with previous observations of an
altered baroreflex working range in hypertensive patients (Gribbin, Pickering, Sleight & Peto,
1971). The locus of the change could possibly be at the baroreceptor level since in animal
experiments a sustained increase in blood pressure is known to cause changes in baroreceptor
threshold and/or sensitivity (McCubbin, Green & Page, 1956).
The manoeuvres known to cause alterations of the muscle nerve SA in normotensive subjects
were tested also in the patients. In general the responses were qualitatively similar in the two
groups, e.g. manoeuvres causing an increase of SA in normal subjects did so in the patients
too. Unusual responses to a manoeuvre were occasionally observed but they were exceptional
findings and a significant relationship to the hypertension seems unlikely.
Skin nerve SA in hypertensive patients
The general pattern of the skin nerve SA recorded in the hypertensive patients was in all
cases similar to that found in normotensive subjects and there was no indication that the
hypertension was associated with a qualitatively altered sympathetic outflow to the skin.
Intra-arterial blood pressure recordings showed no correlation between spontaneous blood
pressure variations and the occurrence of the sympathetic bursts. As in normotensive individuals the strength of the skin nerve SA was altered in response to body cooling and warming.
Changes in the emotional state of the patient also affected the strength of the sympathetic outflow. This was most evident during well-defined periods of mental stress (elicited by suddenly
asking the patient to perform mental arithmetic) which usually resulted in an increase of
activity in a fashion similar the normotensive control.
It must be emphasized that, although well suited to detect temporal variations in the
strength of SA in an unchanged electrode position, the nerve recording method is not well
suited to compare the absolute strength of the neural outflow in different nerve fascicles.
Therefore our impression that it is easier to find strong skin nerve SA in the patients than
in the controls must be regarded as preliminary until more quantitative evidence is obtained.
ACK NO WLEDGMEN TS
We wish to thank Professor B. Hood for valuable support during the investigation. The
investigation was supported by Swedish Medical Research Council Grants Nr B71-14X-2881
02, B72-14X-3546-01and B71-19X-3116-0l.
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