Guest guest Posted June 26, 2003 Report Share Posted June 26, 2003 Caro mentioned Catecholamines and magnesium. In a private email you also mentioned them to me. I had no idea what they were so I did a search on Ask Jeeves and came up with the following! ~~~~~~~~~~~~~~~~~~~~~ Catecholamines- A group of hormones produced by the adrenal glands. They include norepinephrine, epinephrine (adrenaline), and dopamine. They are manufactured from tyrosine. Chapter: 21 Epinephrine and norepinephrine, synthesized and secreted by cells of the adrenal medulla and their neoplastic counterparts. Catecholamines are derived from tryptophan which is converted to a metabolic intermediate, dihydroxyphenylalanine (DOPA). The Catecholamines ---------------------------------------------------------------------------- ---- Possibly the second neurotransmitter to be discovered was initially called sympathetic because it was produced by stimulation of the sympathetic nerves, and it had the opposite effect of acetylcholine on the heart. And like vagusstuf, the name sympathetin was discarded as soon as the chemists got their hands on the sympathetic stuff. The found that it contained a chemical group called a catechol group and an amino group, and were probably all ready to call this neurotransmitter catecholamine when someone, probably an physiologist, noted that the adrenal glands also produced a different chemical called adrenaline that had the same catechol and amino group. So sympathetin couldn't be called catecholamine since there was another. How about noradrenaline? " Wait a minute! " called out an American scientist. " In the good old U.S.A, we call adrenaline epinephrine. That way our ER doctors can say, 'Quick! Inject 10 ccs of epi.right into the heart. Stat!'. So why not call the chemical norepinephrine? " Then it was noted that yet another chemical, dopamine, had the same catechol and amino group as epinephrine and noradrenaline. At which point the chemist decided that he didn't care what the physiologists called these neurotransmitters. Each chemical had both a catechol group and an amino group. They were all catecholamine! And indeed they are. A Happy Family of Neurotransmitters In the beginning there was tyrosine, a common amino acid. All cells are loaded with tyrosine. But all cells, and all neurons, do not make dopamine, norepinephrine and epinephrine. All cells are not catecholaminergic (thank heavens, what a mouthful). Why not? Well, it's in the genes. All cells do not express the genes necessary for the production of the enzymes needed to synthesize the catecholamine neurotransmitters. As you should recall from our discussion of acetylcholine, it's enzymes that determine which neurotransmitter is produced. If a neuron makes ChAT, the cell will produce acetylcholine and be a cholinergic neuron. In the case of the catecholamines, the enzymes are a bit more complicated, but let's see if we can figure it out. All cells contain tyrosine, but only catecholaminergic cells contain the enzyme tyrosine hydroxylase. Tyrosine hydroxylase coverts tyrosine into a chemical that is almost the neurotransmitter dopamine. The chemical is called L-dopa. It takes a second enzyme, a amino acid decarboxylase, to finish the job. All dopaminergic neurons have both of these enzymes and can therefore make dopamine. Cells that make norepinephrine and epinephrine also produce these two enzymes. But they don't release dopamine. Instead, it is quickly converted by another enzyme, dopamine-beta-carboxylase, into norepinephrine. Neurons that have all three enzymes are norepinephrinergic neurons (zounds! what a mouthful). In the CNS and PNS that's the end of story, but to be complete, the adrenal glands have these three enzymes and another, let's just call it enzyme number 4, which converts the norepinephrine into epinephrine before it is released. Thus, the adrenal gland cells are... adrenergic (okay, you could say epinephrinergic. But why?). Four enzymes and some tyrosine and you have a whole family of neurotransmitters. Certainly there must be agonist and antagonists for the family. Catecholamine Receptor Agonists and Antagonists Let's do dopamine first. Dopamine does have several different receptor types. They are called D1, D2, D3, etc. receptors. Really! Sounds like chemists named them to me. And while there are many drugs that act as dopamine agonists and antagonists, all I'd like for you to know is that: L-dopa is the precursor for dopamine. It is used to treat diseases like Parkinson's disease because, unlike dopamine, L-dopa crosses the blood brain barrier. Giving L-Dopa to Parkinson's disease patients works as long as neurons with amino acid decarboxylase are still functioning in the brain. They convert the L-Dopa into dopamine. Dopamine antagonists and often called dopamine blockers. There are D1 blockers and D2 blockers, etc. These are useful in the treatment of diseases with too much like Huntington's chorea. And schizophrenia. Norepinephrine has many agonists, but the one you should know is ... epinephrine. For the most part norepinephrine and epinephrine have the same receptors. Thus each is an agonist for the other. And here's my favorite term, drugs that are agonists for these receptors are called sympatheticomimetic drugs. Because these drugs turn on the sympathetic nervous system just like norepinephrine and epinephrine. When the heart stops, just yell, " 10 ccs of a sympatheticomimetic. Stat! " and look at all the confused faces. There are two different main types of receptors for these neurotransmitters, called alpha and beta receptors. The difference is in the antagonists. Let's keep this simple. Alpha blockers block alpha adrenergic receptors and beta blockers antagonize beta adrenergic receptors. Got it? Degradation of Catecholamines Like acetylcholine, degradation enzymes help to terminate the action of the neurotransmitter. There are two main enzymes which I will merely list without getting into the details -- monoamine oxidase (MAO), and catechol-O-methyl transferase (COMT). Of these, MAO inhibiting drugs are very important in increasing dopamine levels in Parkinson's disease patients. ~~~~~~~~~~~ Depressiion and Catecholamines A New Use for the Amino Acid Phenylalanine Catecholamines Kick Out the Demons of Depression I am in that temper that if I were under water I would scarcely kick to come to the top. - Keats Despair and hopelessness, so characteristic of serious depression, had engulfed the poet Keats when he wrote those words to a friend in 1818. He could not have known then that a chemical called phenylalanine could provide a helpful " kick " for his own soul as well as for many other depressed souls in their struggle to remain afloat. The demons of depression exact a terrible toll on human happiness and productivity - even on life itself. But the quest of science to understand the origins of this affliction, and to ameliorate it, continues to bear fruit. A recent study at the Yale University School of Medicine has shown a strong link between depression and the levels of catecholamines in our bodies.1 That in itself is not news, but there is an intriguing twist. It was found that people who suffer from bouts of clinical depression are biochemically different from people who are normal and healthy. People with a history of clinical depression, even when they are in remission and appear to be healthy, are still biochemically different. They are, in a sense, biochemical time bombs ready to go off into another depressive episode. But what lights the fuse? Perhaps a better question is: Is there a way to dampen the fuse so it fizzles before anything goes boom? Neither question has a simple answer, but much research points to the critical role played by catecholamines. What Are Catecholamines? Catecholamines are biologically active compounds that serve a variety of functions. Dopamine, noradrenaline, and adrenaline are catecholamines. (Noradrenaline and adrenaline are also popularly referred to as norepinephrine and epinephrine.) Dopamine and noradrenaline are neurotransmitters - compounds that mediate the flow of impulses between neurons. Adrenaline is a neurotransmitter responsible for the well-known " fight or flight " response which prepares the body to cope with stress. On its metabolic pathway, the amino acid phenylalanine converts to tyrosine, which transforms to dopamine. Dopamine is the immediate precursor of noradrenaline (see Figure 1). Dopamine deficiency is implicated in some forms of psychosis and abnormal movement disorders, such as Parkinson's disease. Noradrenaline is released by certain neurons in the brain. A disturbance in its metabolism at important brain sites has been implicated in affective disorders. In other words, when noradrenaline is insufficiently present, a person's mood or energy levels may decline, even bottom out - for example, in depression. These simple, structurally similar organic compounds play important roles in regulating the function of our nervous systems, both central and peripheral. Without these molecules, our bodies would be like the Internet if all the modems failed - dead. Normally our bodies synthesize catecholamines from nutrient molecules in our foods. Unfortunately, optimal levels of these nutrients cannot be obtained from food sources alone. One way to ensure sufficient levels of these essential neurotransmitters is by consuming their nutrient precursors via supplementation. Phenylalanine can be taken as a nutrient supplement and neurotransmitter precursor to noradrenaline. Tyrosine does not provide the same uplifting benefits as phenylalanine, because the latter is required for the production of a metabolite, PEA, whose mood-elevating properties augment those of noradrenaline. The Trouble with Catecholamine Deficiency In the randomized, double-blind, crossover study mentioned above, Dr R M Berman and his colleagues at Yale administered a compound, alpha-methylparatyrosine, that inhibits the body's ability to synthesize catecholamines from their chemical precursors. The subjects had a history of clinical depression and had been in remission and medication-free for at least three months. The results were dramatic: depleting the catecholamines produced marked symptoms of depression in the experimental group, as measured by the Hamilton Depression Rating Scale. The control group was almost totally unaffected. The authors concluded that " . . . catecholamine function may play a crucial role in mood regulation for subjects who are vulnerable to depression. " Several earlier short-term studies had shown that inhibition of catecholamine synthesis did not have any effect on the mood of normal, healthy people who had never suffered from clinical depression. They were clearly more resilient than those whose prior depression had made them vulnerable to a temporary depletion of these vital molecules. This does not mean, however, that maintaining optimal levels of catecholamines is not important for normal, healthy people, nor that increased catecholamine levels cannot be perceived in such people. Catecholamines are very important for good mental health, especially as we grow older and our output of these neurotransmitters gradually declines. Most of the mental failings that often accompany aging, such as loss of memory, loss of mental alertness and energy, tendency toward depression, vulnerability to stress, and Alzheimer's and Parkinson's diseases, are associated with reduced levels of noradrenaline or dopamine. There is a growing body of both anecdotal evidence and clinical observations showing that phenylalanine supplements can alleviate the symptoms of some forms of depression. It can also boost various aspects of mental function in healthy people who wish to maximize their ability to stay that way.2 In one such clinical study published in 1984, the authors concluded that " The results support the view that the brain is able to use dietary amino acids to enhance production of brain neuroamines capable of sustaining mood. " 3 It is worth mentioning again that obtaining optimal levels of these neuroamines is not generally feasible with the normal diet alone. Supplementation is required. For the replenishment of noradrenaline, a phenylalanine supplement would be effective. The Orthomolecular Approach Two of the goals of nutritional intervention, as mentioned above - to alleviate the symptoms of disease and to optimize a state of health - exemplify an approach to health care called orthomolecular medicine, or orthomolecular psychiatry when it's aimed at mental disorders. (The prefix ortho is from the Greek orthos = correct.) The underlying idea is that many diseases result from imbalances in the concentrations of certain natural chemicals normally found in the body. These diseases can best be treated by administering one or more of those chemicals or their natural precursors (plus any relevant cofactors) so as to restore the correct balance and therefore restore health. The optimal concentrations of the chemicals needed in the body may differ greatly from the concentrations actually provided by a person's genetic makeup or normal diet, hence the need for nutrient supplementation. The leading figure in the orthomolecular school of medicine was the late Linus ing, one of the greatest scientists who ever lived. Part of ing's legacy is the increasing acceptance of his conviction that the orthomolecular approach to therapy, prophylaxis, and health optimization is generally the best. In his own words, " Significant improvement in the mental health of many persons might be achieved by the provision of the optimum molecular concentrations of substances normally present in the human body. " 4 One way to put this approach into practice is with the Durk Pearson & Sandy Shaw® family of scientifically formulated supplements that contain phenylalanine: Rise & Shine®, Ascend 'n SeeTM, BlastTM, FastBlastTM, Blast CapsTM, and SmartzTM. And remember: if you start feeling down or depressed, it may not be all in your head. You may be able to kick-start your mental energy again just by putting the correct molecules in your stomach. For more information on natural alternatives for helping to alleviate depression, see New and Better Mood Function - July 1999 and DHEA: A Better Antidepressant - July 99 in this issue. For the complete story on these valuable " brain food " supplements, see: Life Enhancement, May 1998 Spring Fever - May 1998 Blast Through Your Walls with Mental Fitness Nutrition - May 1998 Freedom and the Zek's Ant - May 1998 Life Enhancement, December 1998: GET SMARTZ Introducing the World's First Mental Fitness Soft Drink - December 98 - DP & SS Creating SmartzTM Introducing the World's First Mental FitnessTM Soft Drink - December 1998 References Berman RM, Narasimhan M, HL, Anand A, Cappiello A, Oren DA, Heninger GR, Charney DS. Transient depressive relapse induced by catecholamine depletion: potential phenotype vulnerability marker? Arch Gen Psychiatry 1999 May;56(5):395-403. Hendler SS. The Doctors' Vitamin and Mineral Encyclopedia. Simon and Schuster, New York, 1990:225-228. Kravitz HM, Sabelli HC, Fawcett J. Dietary supplements of phenylalanine and other amino acid precursors of brain neuroamines in the treatment of depressive disorders. J Am Osteopath Assoc 1984;84/1Suppl:119-123. ing L. Orthomolecular psychiatry: Varying the concentrations of substances normally present in the human body may control mental disease. J Nutr Environ Med 1995;5/2:187-198. The amino acid tyrosine is the starting material. It is taken up into catecholaminergic nerves by an active transport system. Once inside the nerve, an additional hydroxyl group is added to the aromatic ring of tyrosine by the enzyme tyrosine hydroxylase. Tyrosine hydroxylation is the rate limiting step in the synthesis of catecholamines and is subject to feedback inhibition by the end products. This forms the catechol (dihydroxybenzene) part of the molecule responsible for the family name. The product is dihydroxyphenylalanine (DOPA). Dihydroxyphenylalanine (DOPA) is acted upon by aromatic-L-amino acid decarboxylase. This forms dopamine (DA), one of three naturally occurring catecholamines. DOPA is used to treat certain diseases in which it is desired to increased catecholaminergic transmission at certain sites. DA in catecholaminergic nerves is taken up into synaptic vesicles and is converted to norepinephrine (NE) by the addition of a hydroxyl group on the carbon second (beta) from the amino group (except in a few dopaminergic neurons). Beta hydroxylation is carried out by the enzyme dopamine-beta-hydroxylase (DBH). DBH is located in the synaptic vesicles so the final step in the synthesis of NE occurs in the vesicle in which NE is packaged along with ATP and other material for eventual release. In adrenal medulla cells, NE in the cytosol is acted upon by phenylethanolamine-N-methyltransferase. This adds a methyl group to the amino nitrogen and forms epinephrine (EPI). The addition of a methyl group significantly alters the pharmacology of the catecholamine. Most of the EPI formed in this process is taken into synaptic vesicles and stored for eventual release into the blood stream. The adrenal medulla releases catecholamines into the blood. In humans, catecholamines released from the adrenal medulla are about 80% EPI and 20% NE. Because these catecholamines are released into the blood and act on receptors in target tissues at some distance these catecholamines act as circulating hormones. In summary, synthesis of catecholamines is a multistep process. No wonder, then, that instead of being destroyed they are 'recycled' in large part. Storage of catecholamines Synaptic vesicles actively take up DA, as well as NE (and EPI, if present). Thus, there is a high concentration of catecholamines in synaptic vesicles and a relatively low concentration of catecholamines in the cytosol of catecholaminergic cells. In addition to catecholamines and DBH, some vesicles contain substantial amounts of ATP, ascorbic acid and some specific proteins, chromogranins. Almost all of the catecholamine content of a sympathetically innervated tissue is contained in the synaptic vesicles inside the catecholaminergic nerves. There is a normal background leak of catecholamines out of the vesicles, but the balance is very much in favor of vesicular storage. Reserpine is a drug that inhibits the vesicular catecholamine pump. By preventing the active uptake of catecholamines into the synaptic vesicles, reserpine can result in depletion of catecholamines. This causes some degree of failure of catecholaminergic transmission at essentially all catecholamine junctions because reserpine is a lipid soluble drug that penetrates the blood-brain barrier (BBB). In experimental animals reserpine can cause in essentially total depletion of tissue catecholamines and complete failure of catecholaminergic transmission. At much lower doses in humans, reserpine has been used in the treatment of hypertension. The low concentration of catecholamines in the cytosol of catecholaminergic nerves is maintained in part by the vesicular amine uptake pump and in part by the mitochondrial enzyme, monoamine oxidase (MAO). If cytosolic concentrations of catecholamines increase (for example, as caused by reserpine), then metabolism by MAO inactives them inside the nerve. Thus, reserpine normally results in depletion of catecholamines, not release. Release of catecholamines, means release in physiologically or pharmacologically active form that results in effector organ responses. The MAO metabolites of catecholamines are essentially inactive. Postganglionic sympathetic nerves (except to sweat glands) release mainly NE into the neuroeffector junction. This NE thus acts as a neurotransmitter. Release of catecholamines Nerve-induced release of catecholamines, like synaptic release at other junctions, is based on quantal release of vesicles containing preformed neurotransmitter molecules. Vesicular release depends on depolarization of the nerve terminal and the influx of calcium ion. In ways not yet understood in detail, the influx of calcium promotes simultaneous exocytosis of many vesicles. The release of vesicular contents allows release of catecholamines and ATP (both have short life spans outside the cell) and DBH. The plasma level of DBH has been used as a measure of the turnover of catecholaminergic vesicles, or as a way of trying to quantify the integral of recent sympathetic nerve activity. The release of catecholamines can also be promoted by certain drugs. In the adrenal medulla, ACh acting as the neurotransmitter of the sympathetic ganglion acts on nicotinic receptors and promotes the release of catecholamines into the circulation. Under certain experimental conditions it is possible to mimic this nicotinic effect of acetylcholine not only at the adrenal medulla but at other sympathetic ganglia. Thus, agonists of nicotinic cholinergic receptors of the ganglionic, or neuronal, type (Nn) can cause substantial catecholamine release at postganlionic sympathetic neuroeffectors junctions as well as massive release of catecholamines from the adrenal medulla into the circulation. Dimethylphenylpiperazinium (DMPP) is a classical drug that is a relatively selective agonist of Nn receptors. Epibatadine is a more recent and more selective example. Another mechanism of release of catecholamines is based on an action at the sympathetic nerve terminal. It is not applicable in the adrenal medulla. Indirectly acting sympathomimetic amines such as tyramine, ephedrine and amphetamine are taken up into sympathetic nerve terminals by the amine uptake pump. Normally, this pump serves to inactivate catecholamines in the catecholaminergic neuroeffector juction. However, structurally related compounds can be taken up into the nerve terminal by this transporter. Once inside the catecholaminergic nerve terminal, the indirectly acting sympathomimetic amines cause displacement of catecholamines from storage sites in vesicles, or from other binding sites. The release of catecholamines can be blocked by certain drugs, most notably bretylium (Bretylol®) and guanethidine (Ismelin®). Inactivation of catecholamines Inactivation of the effects of catecholamines at the sympathetic neuroeffector junction can take place by one or more of several mechanisms: uptake or reuptake O-methylation oxidative deamination Uptake or reuptake of catecholamines including NE into (postganglionic) sympathetic nerve terminals is facilitated by an amine uptake pump. This is a part of a family of membrane proteins that transport different transmitter substances across the plasma membrane of the nerve terminal. This pump is driven indirectly by a sodium gradient, which is in turn generated by another plasma membrane protein, the Na+,K+-ATPase, or sodium, potassium 'pump'. The amine uptake pump is selective for NE > Epi but does not take up isoproterenol. Catecholamines which diffuse into the circulation or are released as neurohormones may also be taken up into sympathetic nerve terminals. For example, the small content of epinephrine in postganglionic sympathetic nerve terminals is probably provided by epinephrine from the adrenal medulla that has been taken up. The amine uptake pump is inhibited by cocaine or tricyclic antidepressants, such as imipramine. Uptake of NE is a major mechanism for terminating sympathetic neuroeffector transmission. For this reason, inhibitors of the amine uptake pump potentiate responses to stimulation of the sympathetic nervous system, or to injected compounds that are taken up by the sympathetic nerve terminals. In a sympathetically innervated tissue, such as the heart, the major uptake of catecholamines is neuronal uptake, or so-called uptake-1. An extraneuronal uptake of catecholamines can occur; so-called uptake-2 (not shown). This uptake is into the parenchymal cells of the organ. It is not blocked by cocaine or imipramine. The importance of uptake-2 is uncertain. Both inside catecholaminergic cells, and in the circulation, oxidative deamination of NE is facilitated by the enzyme monoamine oxidase (MAO). The product of the oxidative deamination of EPI or NE is 3,4-didydroxyphenylclyc oaldehyde (DOPGAL). DOPGAL is subject to reduction to the corresponding alcohol (3,4-dihydroxyphenylethylene glycol, DOPEG) or oxidation to the corresponding carboxylic acid (3,4-dihydroxymandelic acid, DOMA); the latter being the major pathway. The product of oxidative deamination of NE (or Epi) is DOPGAL. DOPGAL may be reduced to DOPEG or oxidized to DOMA. Metabolic disposition of catecholamines is important for circulating compounds. Catechol-O-methyl transferase (COMT) plays a major role in terminating catecholamines in the circulation following injection or release from the adrenal medulla. Methylation at the 3 position of the ring of catecholamines is facilitated by COMT. There are no clinically useful inhibitors of COMT. Pyrogallol has been used as an in vitro inhibitor. Final metabolic disposition of catecholamines typically involves the action of both COMT and MAO. MAO is important in regulating the levels of catecholamines in tissues (particularly intraneuronally), but can also act on the 3-O-methyl metabolites of catecholamines (i.e., COMT then MAO). Thus, the major metabolite of norepinephrine and epinephrine that appears in the urine is 3-methoxy-4-hydroxymandelic acid, also called vanillylmandelic acid, or VMA. Metabolic disposition of catecholamine also includes pathways in which COMT acts on the respective MAO-derived metabolites (MAO then COMT). By this process the final product that ends up in the urine is also VMA. ~~~~~~~~~~~~~~~ HOw to test for catecholamines: Catecholamines tests Definition Catecholamines is a collective term for the hormones epinephrine, norepinephrine, and dopamine. Manufactured chiefly by the chromaffin cells of the adrenal glands, these hormones are involved in readying the body for the " fight-or-flight " response (also known as the alarm reaction). When these hormones are released, the heart beats stronger and faster, blood pressure rises, more blood flows to the brain and muscles, the liver releases stores of energy as a sugar the body can readily use (glucose), the rate of breathing increases and airways widen, and digestive activity slows. These reactions direct more oxygen and fuel to the organs most active in responding to stress--mainly the brain, heart, and skeletal muscles. Purpose Pheochromocytoma (a tumor of the chromaffin cells of the adrenal gland) and tumors of the nervous system (neuroblastomas, ganglioneuroblastomas, and ganglioneuromas) that affect hormone production can cause excessive levels of different catecholamines to be secreted. This results in constant or intermittent high blood pressure (hypertension). Episodes of high blood pressure may be accompanied by symptoms such as headache, sweating, palpitations, and anxiety. The catecholamines test can be ordered, then, to determine if high blood pressure and other symptoms are related to improper hormone secretion and to identify the type of tumor causing elevated catecholamine levels. Description The catecholamines test can be performed on either blood or urine. If performed on blood, the test may require one or two samples, depending on the physician's request. The first blood sample will be drawn after the patient has been lying down in a warm, comfortable environment for at least 30 minutes. If a second sample is needed, the patient will be asked to stand for 10 minutes before the blood is drawn. Instead of a venipuncture, which can be stressful for the patient, possibly increasing catecholamine levels in the blood, a plastic or rubber tube-like device called a catheter may be used to collect the blood samples. The catheter would be inserted in a vein 24 hours in advance, eliminating the need for needle punctures at the time of the test. It may take up to a week for a lab to complete testing of the samples. Because blood levels of catecholamines commonly go up and down in response to such factors as temperature, stress, postural change, diet, smoking, obesity, and many drugs, abnormally high blood test results should be confirmed with a 24-hour urine test. In addition, catecholamine secretion from a tumor may not be steady, but may occur periodically during the day, and potentially could be missed when blood testing is used. The urine test provides the laboratory with a specimen that reflects catecholamine production over an entire 24-hour period. If urine is tested, the patient or a healthcare worker must collect all the urine passed over the 24-hour period. Preparation It is important that the patient refrain from using certain medications, especially cold or allergy remedies, for two weeks before the test. Certain foods--including bananas, avocados, cheese, coffee, tea, cocoa, beer, licorice, citrus fruit, vanilla, and Chianti--must be avoided for 48 hours prior to testing. However, people should be sure to get adequate amounts of vitamin C before the test, because this vitamin is necessary for catecholamine formation. The patient should be fasting (nothing to eat or drink) for 10 to 24 hours before the blood test and should not smoke for 24 hours beforehand. Some laboratories may call for additional restrictions. As much as possible, the patient should try to avoid excessive physical exercise and emotional stress before the test, because either may alter test results by causing increased secretion of epinephrine and norepinephrine. Patients collecting their own 24-hours urine samples will be given a container with special instructions. The urine samples must be refrigerated. Risks Risks for the blood test are minimal, but may include slight bleeding from the venipuncture site, fainting or feeling lightheaded after blood is drawn, or blood accumulating under the puncture site (hematoma). There are no risks for the urine test. Normal results Reference ranges are laboratory-specific, vary according to methodology of testing, and differ between blood and urine samples. If testing is done by the method called High Performance Liquid Chromatography (HPLC), typical values for blood and urine follow. Reference ranges for blood catecholamines Supine (lying down): Epinephrine less than 50 pg/mL, norepinephrine less than 410 pg/mL, and dopamine less than 90 pg/mL. Standing: Values for blood specimens taken when the subject is standing are higher than the ranges for supine posture for norepinephrine and epinephrine, but not for dopamine. Reference ranges for urine catecholamines Urine: Epinephrine 0-20 microgram per 24 hours; norepinephrine 15-80 microgram per 24 hours; dopamine 65-400 microgram per 24 hours. Abnormal results Depending on the results, high catecholamine levels can indicate different conditions and/or causes: High catecholamine levels can help to verify pheochromocytoma, neuroblastoma, or ganglioneuroma. An aid to diagnosis is the fact that an adrenal medullary tumor (pheochromocytoma) secretes epinephrine, whereas ganglioneuroma and neuroblastoma secrete norepinephrine. Elevations are possible with, but do not directly confirm, thyroid disorders, low blood sugar (hypoglycemia), or heart disease. Electroshock therapy, or shock resulting from hemorrhage or exposure to toxins, can raise catecholamine levels. In the patient with normal or low baseline catecholamine levels, failure to show an increase in the sample taken after standing suggests an autonomic nervous system dysfunction (the division of the nervous system responsible for the automatic or unconscious regulation of internal body functioning). Terms: Dopamine Dopamine is a precursor of epinephrine and norepinephrine. Epinephrine Epinephrine, also called adrenaline, is a naturally occurring hormone released by the adrenal glands in response to signals from the sympathetic nervous system. These signals are triggered by stress, exercise, or by emotions such as fear. Ganglioneuroma A ganglioneuroma is a tumor composed of mature nerve cells. Neuroblastoma Neuroblastoma is a tumor of the adrenal glands or sympathetic nervous system. Neuroblastomas can range from being relatively harmless to highly malignant. Norepinephrine Norepinephrine is a hormone secreted by certain nerve endings of the sympathetic nervous system, and by the medulla (center) of the adrenal glands. Its primary function is to help maintain a constant blood pressure by stimulating certain blood vessels to constrict when the blood pressure falls below normal. Pheochromocytoma A pheochromocytoma is a tumor that originates from the adrenal gland's chromaffin cells, causing overproduction of catecholamines, powerful hormones that induce high blood pressure and other symptoms. Resources: BOOKS Cahill, . Handbook of Diagnostic Tests. Springhouse, PA: Springhouse Corporation, 1995. s, S. Laboratory Test Handbook. 4th ed. Hudson, Ohio: Lexi-Comp Inc., 1996. Pagana, Kathleen Deska. Mosby's Manual of Diagnostic and Laboratory Tests. St. Louis: Mosby, Inc., 1998. ---------------------------------------------------------------------------- ---- The above information is an educational aid only. It is not intended as medical advice for individual conditions or treatments. Talk to your doctor, nurse or pharmacist before following any medical regimen to see if it is safe and effective for you. This health encyclopedia is made possible by the Dr. ph F. Trust Fund. Dr. was a surgeon who resided in Wausau from 1908 to 1952. In addition to his surgical practice, Dr. possessed a strong commitment to community service and medical education. The agreement which created the Dr. ph F. Medical library was signed in July of 1948. Copyright 1999-2003. The Thomson Corporation. All rights reserved. MyDiseaseDex is a trademark of Micromedex, Inc. Medical Library, 333 Pine Ridge Blvd. Wausau, WI 54401, Phone: , Fax, www.chclibrary.org NEW EMAIL ADDRESS bonnieh4455@... please change from: bheint@... Quote Link to comment Share on other sites More sharing options...
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