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.
Norepinephrine
1. Catecholamine metabolism in thyroid disease
In the same measuredment of the secretion rate
of norepinephrine (NE) in 6 euthyroid subjects, 6 hyperthyroid and 6
hypothyroid patients, infused at a constant rate (0.1 microC/kg/min) for
1 h with tritiated norepinephrine (New England Nuclear Inc.), showed
that the plasma NE secretion rate is normal in hyperthyroidism, and is
significantly elevated in hypothyroidism thereby explaining the higher
plasma NE concentrations seen in hypothyroidism(1).
2. High-dose norepinephrine treatment in critically ill patients
Critically ill patients with circulatory shock
sometimes need rescue treatment with high doses of norepinephrine, a
treatment that may be associated with a poor outcome because of
excessive vasoconstriction. In a retrospective study to evaluate the
outcome of treatment and its determinants in patients with circulatory
shock who received high doses of norepinephrine in the intensive care
unit and to identify indicators of futility for the treatment of 113
consecutive patients with circulatory shock who received 0.9 μg/kg per
minute or greater of norepinephrine during at least 1 hour at any time
in the intensive care unit, found that dose, and duration of
norepinephrine administration did not have prognostic significance.
Scores greater than 40 on the Acute Physiology and Chronic Health
Evaluation II, bicarbonate levels less than 9.0 mEq/L, or receipt of an epinephrine
dose of 0.25 μg/kg per minute or greater were associated with 100%
mortality and concluded that although the cause of shock and treatment
with norepinephrine were not predictive of death when high doses of the
drug were deemed necessary, rescue treatment with high-dose
norepinephrine is futile in patients with severe disease and metabolic acidemia(2).
3. Norepinephrine in Regulation of the Fear Network by Mediators of Stress
In the study of neural modulators, especially those activated during stress, such as norepinephrine (NE), regulate synaptic transmission and plasticity in the network, found that Norepinephrine
(NE) inhibits synaptic transmission in both the subcortical and
cortical input pathway but that sensory processing is biased toward the
subcortical pathway. In addition binding of NE to β-adrenergic receptors
further dissociates sensory processing in the LA. These findings
suggest a network mechanism that shifts sensory balance toward the
faster but more primitive subcortical input(3).
4. Norepinephrine transporter in humans with (S,S)-[11C]O-methyl reboxetine and PET
In a human studies with the PET radiotracer (S,S)-[(11)C]O-methyl reboxetine ([(11)C](S,S)-MRB), a ligand targeting the norepinephrine transporter (NET), found that The highest density of norepinephrine
transporter (NET) was found in the MBR where the LC is located,
followed by THL, whereas the lowest density was found in basal ganglia
(lowest in CDT), consistent with the regional localization of NETs in
the nonhuman primate brain. While all three doses of ATX were found to
block most regions, no significant differences between doses were found
for any region, although the average percent change across subjects of
the MBR did correlate with ATX dose(4).
5. Atomoxetine and attention-deficit/hyperactivity disorder (ADHD)
Atomoxetine is a potent and selective norepinephrine
transporter (NET) reuptake inhibitor acting as a nonstimulant for the
treatment of attention-deficit/hyperactivity disorder (ADHD). In
the study to determine if atomoxetine occupies NET in a dose-dependent
fashion using (S,S)-[18F]FMeNER-D2 in nonhuman primate brain, found that
after administration of atomoxetine, a dose-dependent occupancy from 38
to 82% was observed for various brain regions known to contain high
densities of NET(5).
6. Norepinephrine and Cingulum
The midline and intralaminar thalamic nuclei
(MITN), locus coeruleus (LC) and cingulate cortex contain nociceptive
neurons. The MITN that project to cingulate cortex have a prominent
innervation by norepinephrinergic axons primarily originating from the
LC. Researchers at the Cingulum
NeuroSciences Institute and SUNY Upstate Medical University,, found
that the LC may regulate nociceptive processing in the thalamus. The
well established role of cingulate cortex in premotor functions and the
projections of Pf and other MITN to the limbic striatum suggests a
specific role in mediating motor outflow for the LC-innervated nuclei of
the MITN(6).
7. Dopamine and the norepinephrine transporter
In the testing of the hypothesis that the norepinephrine transporter (NET) is involved in dopamine clearance in the hippocampus,
found that there is very little DAT in this area using ligand binding
with radiolabelled RTI-55. Moreover, in contrast to raclopride (100 μM),
a dopamine D2-autoreceptor antagonist, local administration of the
α2-adrenoceptor antagonist idazoxan (100 μM) increased hippocampal
dopamine. Taken together, our data demonstrate an interaction between
dopamine and norepinephrine systems in the hippocampus. It is proposed that this interaction originates from a shared uptake mechanism at the NET level(7).
8. Norepinephrine stimulate the release of corticotropin-releasing factor-41 from the rat hypothalamus?
In the study the effects of the two putative neurotransmitters acetylcholine and norepinephrine
on immunoreactive CRF-41 release from incubated rat hypothalami, found
that there is an evidence for a stimulatory role of acetylcholine and norepinephrine
on CRF-41 release, and consequently on hypothalamo-pituitary-adrenal
axis in the rat, through actions at a hypothalamic level. The
stimulatory effect of acetylcholine is mediated principally through
muscarinic receptors and that of norepinephrine through beta-adrenoceptors(8).
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Sources
(1) http://www.ncbi.nlm.nih.gov/pubmed/874048
(2) http://www.ncbi.nlm.nih.gov/pubmed/23283085
(3) http://www.ncbi.nlm.nih.gov/pubmed/21647395
(4) http://www.ncbi.nlm.nih.gov/pubmed/17707807
(5) http://www.ncbi.nlm.nih.gov/pubmed/16896954
(6) http://www.ncbi.nlm.nih.gov/pubmed/18317800
(7) http://www.ncbi.nlm.nih.gov/pubmed/21669025
(8) http://www.ncbi.nlm.nih.gov/pubmed/2970959
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