Journal of Human Hypertension (2002) 16 (Suppl 1), S64–S69
 2002 Nature Publishing Group All rights reserved 0950-9240/02 $25.00
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The sympathetic nervous system: the
muse of primary hypertension
V DeQuattro1 and M Feng1,2
Keck School of Medicine, University of Southern California, Los Angeles, California, USA
Von Euler characterised the sympathetic neuro-
transmitter noradrenaline (NA) and postulated that
excessive neural tone was a cause of primary hyperten-
sion (PH). Thirty years ago, we found raised NA levels
in 30– 40% of young patients with PH. Laragh found
plasma renin activity (PRA) a risk marker for coronary
artery disease. With Esler, Miura, and Campese, a close
association was found of plasma NA with PRA. We
found raised tyrosine hydroxylase activity (AC) in the
hearts of a rabbit model of sinoaortic denervated hyper-
tension and in PH with raised plasma NA. Esler utilised
titrated NA infusion and described increased spillover
of NA from heart, kidney and subcortical areas of brain
of patients with PH. With Eide we found raised cerebro-
spinal fluid (CSF) NA in PH (not secondary
hypertension) and with Kolloch and Miura, we found
raised plasma/CSF NA in conjunction with reduced
dopaminergic tone. With Shkvatsabaya, Yurenev and
Davison, we found that relaxation therapy improved the
Keywords: sympathetic nervous system; primary hypertension
Introduction
Muse, one of the nine daughters of the Greek Gods
of mythology – Mnemosynl and Zeus, is a guiding
spirit or influence over one of the Arts and Sciences.
In our view, the sympathetic nervous system (SNS)
is the Muse over the circulatory system, and thus a
major influence or cause of primary hypertension.
The evidence seems to indicate that the control of
raised blood pressure begins in the brain, probably
in the hypothalamus. Recent work by Campese et al1
indicates that a drop of phenol on the kidney can
elicit a central noradrenergic pressor response. So
that a central outflow of increased SNS activity may
not be the initiating factor in blood pressure elev-
ation, but that it may reside in a peripheral organ or
vessel. So we will leave open where it actually
starts, though we believe that the SNS plays an
important role as a causative factor in primary
hypertension, and is also a major factor in the gen-
esis of the complications of hypertension, including
ischaemic heart disease, congestive heart failure
Correspondence: V DeQuattro, MD, Keck School of Medicine,
University of Southern California, Los Angeles, CA, USA
2
M Feng, MD, Visiting Scholar, People’s Republic of China
anger ambience and blood pressure of PH with raised
plasma NA vs those with normal NA levels. Campese
found a hypothalamic source of raised blood pressure
in two rat models – microphenol treated and ischaemic
kidney. The resulting hypertension was associated with
raised NA turnover of their hypothalamic centres.
Finally, with Hsueh and Hodis, we found raised plasma
NA in association with insulin resistance increased left
ventricular mass and intimal medial hypertrophy in Mex-
ican-American diabetics and their yet unaffected off-
spring. Reliable estimates of human sympathetic AC,
including levels of plasma NA in the effluent of selected
organs and peripheral venous and arterial sites, may
eventually be displaced by techniques using genetic
analysis and molecular biology. Never the less, the sym-
pathetic nervous system appears to play an important
role in the pathogenesis, sequelae and therapy of PH.
Journal of Human Hypertension (2002) 16 (Suppl 1), S64–
S69. DOI: 10.1038/sj/jhh/1001346
(CHF), atherosclerotic cardiovascular disease, and
renal dysfunction.
SNS activity in the clinical setting
There are several ways to assess SNS function in the
patient with hypertension or with other types of
adrenergic dysfunction. Spectroanalysis can be used
for heart rate and RR variability, baroceptors testing,
valsalva manoeuver, depressor responses to sym-
pathoplegic agents, heart rate response to posture –
that is often a bedside indicator of the SNS activity,
whether it is paramount, present, or absent in
patients with postural hypotension. Cardiac cat-
echolamine (CA) turnover has been measured by
Goldstein et al2 and other workers using fluro-
dopamine uptake and turnover or flurodesoxyglu-
cose. These techniques appear to offer a quantitative
assay of cardiac noradrenaline (NA) content and
turnover in autonomic disorders before and after the
effects of various drugs. Systolic time intervals have
also been used to characterise the disordered SNS
function. For years blood CA, generally measured in
an antecubital vein, reflects CA produced by the
nerve ending and via the synapse entering the
venous circulation. This is an averaging of nor-
adrenergic activity to that limb. Relative contributors

of the limb or an organ to the circulation may be
obtained from both arterial and venous sampling.
Murray Esler,3 went further in these assessments by
measuring NA spillover rates using both the
endogenous level of CA and the level of radiolabel
after graded infusion.
Dopa, dopamine and the metabolites
What is the role of dopamine (DA)? Is it a precursor
to NA or does it represent some other activities of
the central or peripheral SNS. And also the CA
metabolites – which serves best to assess SNS func-
tion? The primary metabolite used to detect or rule
out pheochromocytoma are the plasma levels of the
metanephrines. Plasma levels of metanephrines
have replaced the urinary levels as the more sensi-
tive test. In fact, other precursors and metabolites,
dihydroxyphenylalanine, dihydroxyphenylglycol,
dihydroxyphenylacetic acid, and dihydroxymand-
elic acid, can give an indication of SNS activity.4
But, it is important to keep in mind that the neuro-
transmitter, NA, is present in the nerve ending of
the SNS, and along with adrenaline (A) in the
adrenal gland, the latter in a ratio of A:NA of about
3 or 4 to 1. This ratio is helpful in localising pheoch-
romocytomas using venous sampling. The major
metabolite of the CA is vanilmandelic acid (VMA).
However, VMA excretion is often normal in patients
with pheochromocytoma, and usually the CA and
normetanephrines are the best reliable assay. Often,
the only metabolite that is elevated in pheochromo-
cytoma are the metanephrines, especially in patients
with malignancy.
Raised plasma catecholamines (CA)
One of the first papers on plasma CA in primary
hypertension was from LAC+USC Medical Center. It
was almost 30 years ago on the Surgical Wards at
LA County where we studied patients with primary
hypertension and age-matched normal volunteers.
We found increased CA levels – about 30% higher
in the hypertensive patients than in controls – after
the patients were supine for an hour while resting
comfortably and with an indwelling line. This was
the second report of a raised level of CA in primary
hypertension.5 The first paper preceded ours by 2
years using the double isotope assay of Engleman
and Lovenberg.6 We studied 27 patients and seven
(27%) had raised CA. At that time therefore, we pos-
tulated that there are some patients with primary
hypertension whose SNS is over active and contrib-
utes to blood pressure elevation.
These were generally younger people and the
studies therefore were extended by ourselves and
others over the next 10 years. Various contributors
found very similar results when they measured
plasma CA in patients with primary hypertension.
Many of these scientists had worked with us – Dr
Miura in Sendai, Dr Esler who was then at Ann
The sympathetic nervous system
V DeQuattro and M Feng
S65
Arbor and now at the Baker Institute in Australia,
Dr Eide in Oslo Norway, Dr Kobayashi in Sendai,
and Dr Kolloch in Bonn. All of these people reported
results similar to our findings of 30 years ago. In
summary, the theory was: somewhere in the central
nervous system, probably central command in the
bedroom of the brain – the hypothalamus, was sti-
mulating peripheral nerves and raising NA levels.
We believed that the increased SNS tone caused the
blood pressure elevation in some patients with
hypertension.
Myths, muses and neurogenic factors
One of the earliest meta-analyses in cardiovascular
medicine was that done by David Goldstein at NIH.
He evaluated 32 published studies and found that
plasma NA or CA levels were elevated in 80% of
them, and in 40% there was a significant rise in
plasma NA or CA in patients with primary hyperten-
sion.7 Thus, younger hypertensive patients have
raised NA levels. Is that just anxiety? That led my
colleague, Yukio Miura, one of a long line of
coworkers from Sendal and myself in our paper in
1973 to address the question ‘Neurogenic factors in
primary hypertension: mechanism or myth’.8
Amaterasu Ohmikami – mythology, and later its
adoption into the Shinto religion holds that the birth
of the Japanese nation and the divine linking of the
emperors to the Sun Goddess, Amaterasu, started
when her grandson became the father of the first
emperor. Thus, a mysterious but powerful woman
was believed to be the Muse of the nation of Japan.
This myth/belief was removed officially by the
Allied command in 1945, but it flourishes in some
circles.
Noradrenaline, renin and cardiac output
Is the SNS a more powerful Muse than renin? In
1970, John Laragh, after measuring plasma renin in
patients with hypertension, found that some
patients with high renin had a greater morbidity
from heart attack than those with low renin. Sub-
sequently, Laragh et al followed patients for 10 years
and examined their heart attack rate along with
blood glucose and renin profiling.9 The interaction
of renin and cholesterol revealed that in patients in
whom both values were high, event rates were high-
est; conversely, they were low in patients with the
opposite profile. That renin is predictive of morbid
events has been validated with the advent of the car-
dioprotective angiotensin-converting enzyme
inhibitory.
Murray Esler (who was working in Julius’ lab in
Ann Arbor where raised cardiac output was found
in young patients with primary hypertension) and
I measured both renin and catecholamines, cardiac
output, peripheral resistance and behavioural fac-
tors in young patients with hypertension. We found
that the patient with the higher plasma renin
Journal of Human Hypertension
 The sympathetic nervous system
V DeQuattro and M Feng
S66
activity (PRA) had higher cardiac output, heart rate,
peripheral vascular resistance and ‘anger in’.10
Further, the CA levels were raised in these patients
compared with the normal subjects and the normal
renin patients.10 In addition, Miura et al11 studied
patients at both the Los Angeles County and the
White Memorial Medical Center. We again found
that plasma NA levels of high renin patients
exceeded those of the other patients. Systolic time
intervals, cardiac index, and heart rate were also
increased. Julius and Esler, examining depressor
responses to sequential autonomic blockade via
renin status (atropine then propranolol then the
alpha blocker phentolamine), found that patients
with high renin had greater reductions in mean
blood pressure with total autonomic blockade, sug-
gesting an adrenergic role for blood pressure elev-
ation.10 High heart rate, perhaps reflecting high SNS
tone is predictive of increased coronary risk. There
were strident non-believers in plasma CA as a SNS
marker. In fact, Folkow had said ‘not so seldom it is
about as difficult to judge a differentiated sympath-
etic activity from plasma noradrenaline levels as it
is to judge from a beach the size, speed and direction
of a ship passing beyond the horizon by means of
the swells that it delivers at the beach line’. This
was his way of saying I do not believe it.
Animal models, human tissue, and CSF
studies
In the 1960s with Alexander and Nagatsu here at
USC, we studied our first hypertensive animal
model, the sino aortic denervated rabbit. Later we
studied the rat Goldblatt and Okamoto SHR models,
and human hypertensives vas deferens. We also
studied central SNS function via the cerebrospinal
fluid (CSF) in human hypertensive patients; with
either primary hypertension, pheochromocytoma, or
renovascular disease. We looked for a neurogenic
role in primary hypertension by measurements of
spinal fluid CA and metabolites and other neurologi-
cal functions. We assessed plasma prolactin and
dopamine centrally (CSF) and peripherally (blood).
We used the dopamine agonist bromocriptine to
stimulate the dopaminergic system.
SAD model
It was found that cardiac NA and protein synthesis
increased within 2 days in rabbits who had their
buffer nerves severed12 and also that within 2 days
left ventricular mass along with protein synthesis
increased consonant with a prompt rise in sympath-
etic activity in this model, akin to human labile
hypertension. The lability of the hypertension
depended in part on the ambient environment of the
animal. This was the initial finding of raised NA
synthesis in an animal model of hypertension,
Journal of Human Hypertension
Human vas deferens
Similar biochemical attributes of SNS function were
found in human vas deferens of patients with pri-
mary hypertension whose tissues were being
removed for elective sterilization. With Bob Men-
dez13 we found that plasma CA and tissue levels of
NA were both raised and CA biosynthesis activity
was increased. The rate limiting step, tyrosine
hydroxylase activity, was also increased.
CSF NA and signals from the brain
We found CSF NA levels were higher than the
respective levels in the plasma of patients with pri-
mary hypertension.14 On the other hand, in patients
with phenochromocytoma the levels of CA were
much lower in the spinal fluid than they were in the
plasma. Thus there appeared to be no penetration of
the blood brain barrier by the CA in the blood of the
patients with pheochromocytoma. Our findings with
metanephrines in CSF and plasma were similar:
they were elevated in patients with primary hyper-
tension.15 Plasma and CSF DA were lower in pri-
mary hypertensives compared with normoten-
sives.16 Young hypertensives with raised NA had
greater blood pressure and plasma NA reductions to
the dopamine agonists bromocriptine, suggesting
that these patients had impaired dopaminergic con-
trol and secondarily heightened SNS function; anal-
ogous perhaps to Parkinson’s disease wherein poor
dopaminergic control within the basal ganglia of
patients leads to tremor and motor dysfunction. Per-
haps in the hypothalamus impaired dopaminergic
stimulation leads to enhanced NA in patients with
primary hypertension.17 These findings and the
many other contributions of our colleagues from
Japan, Sato, Nagatsu, Miura, Kobayashi, and
Kimura, suggest to me that perhaps the SNS Muse
and Amaterasu are one and the same.
Esler initiated studies of NA spillover to measure
general SNS activity, as well as that of specific
organs.10 He assessed central SNS function in
human hypertension by measures of catecholamine
spillover in both jugular veins. He found that the
major jugular vein drained the superior saggital
sinus, and the right jugular vein drained the basal
ganglia mid brain and hypothalamus.18 He found
elevated NA spillover coming from the hypothala-
mus areas. He found similar results in patients with
CHF, suggesting that in the patient with CHF the
well spring of the sympathetic activity is in the
hypothalamus, probably in response to their low left
ventricular filling pressures and the high pulmonary
artery pressures.
Noradrenergic behaviour and relaxation
therapy
We studied the source of the sympathetic storm
early on with Kiley and his colleagues in the psy-

chiatry department at LA County/USC. We exam-
ined flight and fight responses in patients with
hypertension, looking at their responses to noxious
tasks and their behavioural ambience of anxiety,
anger, and depression. We found that primary
hypertensives had more anxiety, depression, and
anger than normotensives. Patients with secondary
hypertension had the same psychological features as
normal volunteers. Thus, there seems to be a differ-
ent psychological ambience in patients with primary
hypertension. We characterised which of our
patients were type ‘A’ personality, the joyless, striv-
ing categorisation of Ray Rosenmen, and then we
attempted to lower their blood pressure with relax-
ation therapy. We espoused an adrenergic hypoth-
esis for some of these patients as well. We looked at
the influence of behaviour on patients with hyper-
tension.
In 1982, with Shkhvatsabaya, Yurenev, and
Salenko in the Myasnikov Institute of Cardiology in
Moscow, we assessed the influence of a relaxation
therapy technique of SNS tone, blood pressure and
left ventricular mass.19 Using relaxation therapy, we
controlled blood pressure and reversed left ventricu-
lar mass in some patients with hypertension. We
brought their technique to USC, and with the assist-
ance and modifications by Davison in the psy-
chology department at USC, we found that patients
with raised levels of NA had greater anger and hos-
tility.20 Relaxation training methods to these
patients resulted in greater reductions of blood
pressure, heart rate, and anger thoughts.21 Thus, it
appeared amazing that a simple technique like
learning how to relax can really reduce both abnor-
mal behaviour and blood pressure.
The diary of a type A patient; see the boss early,
sales meeting confirmed, get out the order no matter
what, hurry up; this is a real diary of a patient who
died at 8.00 that evening probably at the PTA meet-
ing. We divided our patients into type A and B
according to his structured interview and we did
find that the type A patients had a greater left ven-
tricular mass than the type B patient and raised NA
levels. There have been other studies in animals
relating NA to hypertrophy of the heart. The
researchers at Harbor UCLA had an animal model
of left ventricular hypertrophy involving only septal
hypertrophy. This was obtained by using NA
infusions at low levels so that the dogs did not
develop hypertension, but did develop hypertrophy
of their septum and left ventricle. We believe that
type A subjects have behaviour patterns of striving
which leads to increased sympathetic tone, and
therefore organ changes of left ventricular hyper-
trophy independent of the blood pressure.
Spells, autonomic features, impaired
oxidative deamination
Some patients with raised adrenergic features serve
as caricatures – mimicking pheochromocytoma. One
The sympathetic nervous system
V DeQuattro and M Feng
S67
example is a lady that was ‘rule out pheochromo-
cytoma’. I first saw her when I came into the examin-
ing room and she had already disrobed because ‘I
am burning up’. Her face was red and hot, both her
blood pressure and heart rate were elevated. Many
similar patients are referred to us to ‘rule out’
pheochromocytoma – they are sweating, flushing
and have other autonomic features. The work-up
does not reveal a pheochromocytoma. This clinical
presentation demands a differential diagnosis to
exclude thyroid and serotonin disorders, but some
probably do have ‘hyperadrenergic’ spells. Irvine
Page described patients with these features over 60
years ago as ‘diencephalic epilepsy’ simulating a
tumor in the diencephalon. Many of his patients
were women with paroxysmal hypertension and
profound autonomic features. Thus, in some
patients, the adrenergic spells may represent norad-
renergic fits that arise in the hypothalamus.
Approximately 10% of our referred patients had
very low levels of VMA despite high levels of met-
anephrines in the urine. The dominant ratio of
amines to acid metabolites suggested that these were
taking a monoamine oxidase inhibitor.22 As in
Page’s syndrome, these patients are predominantly
women with prominent flushing, tachycardia, labile
hypertension and raised plasma NA. The biochemi-
cal and clinical features may be linked to oes-
trogen dysregulation.
Noradrenergic genesis of ischaemic
heart disease and CHF
We wished to examine the role of the SNS in
ischaemic heart disease. Earlier, Horwitz and
Sjoerdsma23 described patients who developed ST
segment depression first on exercise and then a rise
in the blood pressure. This suggested that some
patients with ischaemic heart disease have hyper-
tension secondary to coronary ischaemia.23 James
described an area of the heart in the septum called
‘the body of James’. Hypoxia leads to platelet release
of serotonin, stimulation of these cardiac chemo-
receptors and activation of afferents to the brain
which raises central SNS activity, blood pressure
and heart rate. Generally, a patient who is hyperten-
sive, because of increased blood pressure and heart
rate product, encounters ischaemia when coronary
perfusion is limited. However, there are some
patients who have ischaemia, and subsequently the
SNS seems to be activated. Thus, there are several
possible roles for SNS in patients with stable angina.
We measured ambulatory blood pressure, real time
ischaemia, and using an automated device which
draws blood when the patients is having an
ischaemic episode, we found that CA levels were
raised in the silent ischaemic attack. We prevented
the angina in these patients with beta-blocker ther-
apy.24 Oral immediate release nifedipine therapy
was not very effective.25 Thus, in most of our
patients with stable angina, SNS stimulation pre-
Journal of Human Hypertension
 The sympathetic nervous system
V DeQuattro and M Feng
S68
ceded the rise in blood pressure, heart rate and ST
segment depression, and it could be modulated with
metoprolol therapy.
We worked with Elkayam in Los Angeles and Losa
in Argentina. Patients with Chagas induced CHF
had lower plasma CA levels related to Chagasic
denervation.26
The higher the level of CA in CHF, the higher the
SNS influence and the poorer the prognosis. Drugs
such as carvedilol and metoprolol can block and
shield the way of sympathetic influence and allow
the myocyte to come back more to its adult function.
Plasma CA levels are related to muscle sympathetic
nerve activity, and predict an earlier demise in
patients with CHF. Cardiac muscle release of CA can
be assessed in the coronary sinus: coronary sinus CA
are increased more in hypertensive patients and are
greater in hypertensives with left ventricular
hypertrophy and highest in those with hypertrophic
cardiomyopathy. Thus, there appears to be a role for
SNS dysfunction in the hypertrophy process.
Conclusion
John Laragh made the astute observation that hyper-
tensive patients had different biochemical and
haemodynamic qualities, and those with high renin
were at great risk. More recent demographic studies
by Julius demonstrate that patients with high renin
tend also to have a higher cholesterol, NA and sys-
tolic blood pressure.27 Approximately 20% of their
patients had high plasma renin. We described a 27–
30% incidence of raised catecholamine in patients
with primary hypertension. NA and cholesterol
levels both increase in response to postural chal-
lenge. Thus, SNS activity can adversely influence
cholesterol levels and metabolism, and therefore the
SNS can crucially activate coronary risk. John Lar-
agh and his colleagues have provided solid evidence
that plasma renin activity is a marker for cardio-
vascular risk. Studies of ischaemic heart disease
morbidity with ACE inhibitors or beta-blockers
show important cardioprotection. Thus, it is still
plausible and possible that the SNS is the dog wag-
ging the tail of the renin angiotensin system. Julius
has described the relationship of the SNS to left ven-
tricular hypertrophy, independent of blood press-
ure, leading to arrhythmia, sudden death, a
reduction of plasma volume (as in patients with
pheochromocytoma), increased vascular hypertro-
phy and changes in haematocrit and blood platelets
contributing to thrombosis, coronary spasms, insu-
lin resistance, dyslipidaemia, and thus coronary
heart disease.28 Thus the SNS is a major player in
coronary risk. Heart rate, a risk marker of adrenergic
tone is related to insulin resistance. Additional stud-
ies found increased alpha-1 adrenergic tone in
patients with syndrome X. We assessed the morning
pressure surge in patients with hypertension and
demonstrated that it could be blunted with an alpha
and beta-blocker, labetalol.29
Journal of Human Hypertension
In studies with Hsueh and Hodis, we related car-
diovascular sequelae to SNS tone and to insulin
resistance.30 We studied Mexican American families
with diabetes, the offspring were not involved, 25
were hypertensive. Diastolic blood pressures were
related to noradrenaline levels. Patients with higher
plasma NA had greater left ventricular mass index
and intimal medial thickness. Patients with insulin
resistance also had a greater left ventricular mass
index. Thus, in these families insulin resistance and
SNS tone appeared related to cardiovascular damage
as well as salt sensitivity. There may be a link to an
abnormal beta-3 adrenergic receptor and work is in
progress in that area.
Summary
Our task for the past 35 years has been to assess SNS
function in the clinical setting often utilising plasma
NA as a sensitive, reproducible, readily available
and inexpensive invaluable marker. Generally, NA
spillover measurements are superior in aspects of
specificity and regionality, but the technical avail-
ability is constrained by the inherent nature of the
methodology. Perhaps genetic analysis and the mol-
ecular biology of the new millennium will replace
these older methods. Current evidence supports
neurogenic factors as causative in the genesis and
sequelae of some patients with primary hyperten-
sion. Despite its limitations, plasma NA may con-
tinue to provide a marker for SNS tone, and further
it may just be possible from the ripples on the beach
to tell the speed, direction and size of a passing ship
unseen beyond the waves.31 The SNS muse has a
powerful influence on the cardiovascular system.
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