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Sunday, 15 December 2013

The Effects of Hormone Catecholamines - Norepinephrine (1)

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 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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