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Saturday, 14 December 2013

The Effects of Hormone Amine - Catecholamines

. 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