. Catecholamines, derived from the amino acid tyrosine, produced
by the adrenal glands, which are found on top of the kidneys. are
epinephrine (adrenaline), norepinephrine (noradrenaline) and dopamine.
The hormone are released into the blood during times of physical or
emotional stress.
1. Catecholamine and dorsolateral prefrontal cortical networks
The symptoms of attention-deficit/hyperactivity disorder (ADHD) involve
impairments in prefrontal cortical top-down regulation of attention and
behavior. In the study of Catecholamine
influences on dorsolateral prefrontal cortical networks, conducted by
Yale University School of Medicine, indicated that the stimulant
medications and atomoxetine appear to enhance PFC function by indirectly
increasing these catecholamine actions
through blockade of norepinephrine and/or dopamine transporters. In
contrast, guanfacine mimics the enhancing effects of norepinephrine at
postsynaptic α(2A)-receptors in the PFC, strengthening network
connectivity. Stronger PFC regulation of attention, behavior, and
emotion likely contributes to the therapeutic effects of these
medications for the treatment of ADHD(1).
2. SRY regulation of catecholaminess and The male fight-flight response
According to the study
by Brain and Gender, Prince Henry's Institute of Medical Research, The
SRY gene, which is located on the Y chromosome and directs male
development, may promote aggression and other traditionally male
behavioural traits, resulting in the fight-or-flight reaction to stress(2).
3. Caffeine on the levels of brain serotonin and catecholamine
Caffeine, a stimulant, which can prompt lipolysis, has been applied on the therapy of obesity. In the study to measure The brain
neurotransmitters levels and body fat content At 12-week of age, obese
mice and their lean counterparts (+/?) were administered with caffeine
(4 mg/d) in water for 4 weeks, showed that the obese mice without
caffeine treatment had lower brain norepinephrine and epinephrine levels than the lean controls. And there had no difference between obese and lean mice in brain
levels of serotonin, tryptophan, and 5-hydroxyindoleacetic acid.
Caffeine treatment showed no effect on the food intake, but decreased
the body fat content significantly in obese mice(3).
4. Dietary copper supplementation influences the catecholamine levels
In the study to investigate the effects of dietary Cu supplementation on the catecholamine
levels in genetically obese mice, male obese (ob/ob) mice and their
lean (+/?) counterparts, with either a control diet (4.0 mg/kg) or a
Cu-supplemented diet (50 mg/kg) for 4 wk, researchers at the Taichung
Veterans General Hospital, showed that catecholamine
levels in ob/ob mice can be increased by dietary Cu supplementation.
However, the interaction between Cu and sympathetic nervous activity in
obesity was not elucidated in this study(4).
5. The effects of dietary protein source on serotonin and catecholamine synthesis rates
In the study of fed rats single meals, containing one of 5 proteins
(zein, wheat gluten, soy protein isolate, casein, lactalbumin, 17% by
weight) or no protein, and killed them 2.5 h later, 30 min after the
injection of m-hydroxybenzylhydrazine, to allow serotonin and catecholamine synthesis rates to be measured in brain, showed that tryptophan concentrations and serotonin synthesis in brain neurons are remarkably sensitive to which protein is present in a meal. Conceivably, this relationship might inform the brain about the nutritional quality of the protein ingested(5).
6. The role of glucose, oxygen and epinephrine resuscitation
In the study of Cholinergic alterations and its further complications in
learning and memory due to hypoxic insult in neonatal rats and the
effect of glucose, oxygen
and epinephrine resuscitation, showed that the reduction in
acetylcholine metabolism is indicated by the down regulated choline
acetyltransferase and up regulated acetylcholine esterase expression.
These cholinergic disturbances were reversed to near control in glucose
resuscitated hypoxic neonates. The adverse effects of immediate
oxygenation and epinephrine administration are also reported. This has
immense clinical significance in establishing a proper resuscitation for
the management of neonatal hypoxia(6).
7. Endocrine regulation of neonatal hypoxia
In the study to assess and focus on changes in insulin and
triiodothyronine concentration in serum, its receptors in the hearts of
hypoxic neonatal rats and glucose, oxygen,
and epinephrine resuscitated groups, found that the insulin
concentration was significantly increased with a significant
upregulation of receptors in hypoxic neonates. Triiodothyronine content
and its receptors were significantly decreased in serum and the hearts
of hypoxic neonates. The change in hormonal levels is an adaptive
modification of the endocrine system to encounter the stress. The
effectiveness of glucose resuscitation to hypoxic neonates was also reported(7).
8. Enhanced brain stem 5HT₂A receptor function under neonatal hypoxic insult
Molecular processes regulating brain stem
serotonergic receptors play an important role in the control of
respiration. In the study to evaluate the 5-HT(2A) receptor alterations
in the brain stem of neonatal rats exposed to hypoxic insult and the effect of glucose, oxygen,
and epinephrine resuscitation in ameliorating these alterations, found
that Hypoxic stress increased the total 5-HT and 5-HT(2A) receptor
number along with an up regulation of 5-HT Transporter and 5-HT(2A)
receptor gene in the brain stem of neonates. These serotonergic alterations were reversed by glucose supplementation alone and along with oxygen to hypoxic neonates. The enhanced brain
stem 5-HT(2A) receptors act as a modulator of ventilatory response to
hypoxia, which can in turn result in pulmonary vasoconstriction and
cognitive dysfunction. The adverse effects of 100% oxygenation and
epinephrine administration to hypoxic neonates were also reported(8).
9. Catecholamine-releasing action in guinea-pig papillary muscles
In the study to investigate wheather tetraethylammonium ion (TEA)
prolongs the action potential (AP) was examined by standard
microelectrode techniques in papillary muscles
isolated from nonreserpinized and reserpinized guinea-pig hearts,
showed that TEA modifies its intrinsic prolonging action of the AP by
releasing norepinephrine from sympathetic nerve terminals; TEA prolongs
the AP by reducing the time-independent outward current rather than the
time-dependent outward current; and a TEA-sensitive current does not
effectively contribute to the total ionic current at the time of
Vmax(9).
10. The Effects of hypertension on cardiovascular responses to epinephrine
Cardiac beta-receptor responsiveness is diminished by both aging and
hypertension. In the study to evaluate of14 young and 18 older
normotensive men and women and in 10 young and 17 older hypertensive men
and women by echocardiography cardiac responses to intravenous infusion
of epinephrine and to assess the relative contribution of intrinsic
cardiac and counterregulatory components to the overall respons, found
that Epinephrine-induced increases in heart rate were similar in the four groups. Increases in stroke volume,
ejection fraction, and cardiac index were similar in the two
hypertensive and two young normotensive groups. In contrast, they were
attenuated in the older normotensive group, resulting in higher left
ventricular responses in older hypertensive than in normotensive
subjects. Heart rate and left ventricular
responses to epinephrine in the presence of ganglionic blockade did not
differ between the two young groups. Increases in plasma norepinephrine
due to epinephrine infusion were larger in hypertensive than in
normotensive subjects(10).
11. Epinephrine, vasodilation and hemoconcentration in syncopal, healthy men and women
In the study to evaluate why healthy young people may become syncopal
during standing, head up tilt (HUT) or lower body negative pressure
(LBNP by measuring the hormonal indices of autonomic activity along with
arterial pressure (AP), heart rate (HR), stroke volume (SV), cardiac output (CO), total peripheral resistance (TPR) and measures of plasma volume,
found that the presyncopal decline in blood pressure in otherwise
healthy young people resulted from declining peripheral resistance
associated with plateauing norepinephrine and plasma renin activity,
rising epinephrine and rising blood viscosity. The increased
hemoconcentration probably reflects increased rate of venous pooling rather than rate
of plasma filtration and, together with cardiovascular effects of
imbalances in norepinephrine, epinephrine and plasma renin activity may
provide afferent information leading to syncope(11).
12. Adrenal glands and the activation of glucogenesis during undernutrition
In adults, the adrenal glands are essential for the metabolic response
to stress, but little is known about their role in fetal metabolism. In
the study to investigate the effects of adrenalectomizing fetal sheep on
glucose and oxygen metabolism in utero in fed conditions and after
maternal fasting for 48 h near term, showed that the circulating
concentrations of cortisol and total catecholamines, and the hepatic glycogen
content and activities of key gluconeogenic enzymes, were also less in
AX than intact fetuses in fasted animals. Insulin concentrations were
also lower in AX than intact fetuses in both nutritional states.
Maternal glucose utilization and its distribution between the fetal,
uteroplacental, and nonuterine maternal tissues were unaffected by fetal
AX in both nutritional states. Ovine fetal adrenal glands, therefore,
have little effect on basal rates of fetal glucose and oxygen metabolism
but are essential for activating fetal glucogenesis in response to
maternal fasting. They may also be involved in regulating insulin
sensitivity in utero(12).
13. Catecholamine concentrations in hyperthyroidism and hypothyroidism
In the study to measure the plasma epinephrine
(E) and norepinephrine (NE) concentrations in patients with thyroid
dysfunction, showed that hyperthyroidism is accompanied by normal plasma
NE concentrations and that hypothyroidism is associated with
significantly increased plasma NE concentrations, possible in an attempt
to compensate for the lack of thyroid hormones(13).
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Sources
(1) http://www.ncbi.nlm.nih.gov/pubmed/21489408
(2) http://www.ncbi.nlm.nih.gov/pubmed/22408002
(3) http://www.ncbi.nlm.nih.gov/pubmed/8039038
(4) http://www.ncbi.nlm.nih.gov/pubmed/8962796
(5) http://www.ncbi.nlm.nih.gov/pubmed/19454292
(6) http://www.ncbi.nlm.nih.gov/pubmed/21907834
(7) http://www.ncbi.nlm.nih.gov/pubmed/21846315
(8) http://www.ncbi.nlm.nih.gov/pubmed/21484469
(9) http://www.ncbi.nlm.nih.gov/pubmed/3785438
(10) http://www.ncbi.nlm.nih.gov/pubmed/17307999
(11) http://www.ncbi.nlm.nih.gov/pubmed/11695710
(12) http://www.ncbi.nlm.nih.gov/pubmed/20959526
(13) http://www.ncbi.nlm.nih.gov/pubmed/958003
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