what does norepinephrine do?
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It is a neurotransmitter in the catecholamine family that mediates chemical communication in the sympathetic nervous system, a branch of the autonomic nervous system. Like other neurotransmitters, it is released at synaptic nerve endings to transmit the signal from a nerve cell to other cells. Norepinephrine is almost identical in structure to epinephrine, which is released into the bloodstream from the adrenal medulla under sympathetic activation. The sympathetic nervous system functions in response to short-term stress; hence norepinephrine and epinephrine increase the heart rate as well as blood pressure. Other actions of norepinephrine include increased glycogenolysis (the conversion of glycogen to glucose) in the liver, increased lipolysis (the conversion of fats to fatty acids; in adipose (fat) tissue, and relaxation of bronchial smooth muscle to open up the air passages to the lungs. All of these actions represent a mobilization of the body's resources in order to meet the stressful challenge–such a response is often termed the "flight or fight" syndrome.
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Antihistimine. It is also used to treat depression.
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Neurotransmitters - What They Do . . .\n\nNeurotransmitters are small molecules whose function is to transmit nerve signals (impulses) from one nerve cell (neuron) to another. Neurotransmitters are chemical messengers which neurons use to tell other neurons that they have received an impulse. There are many different neurotransmitters - some trigger the receiving neuron to send an impulse and some stop it from doing so. See this simplified diagram of a neuron: \n\n\nNerve impulses always flow in one direction - from the branched extensions called dendrites, down the neuron to the presynaptic terminals. The join between the presynaptic terminals of one neuron and the dendrites of another is called the synapse. \n\nThe two neurons do not actually touch each other but are separated by a space called the synaptic cleft. \n\nWhen a nerve impulse arrives at a presynaptic terminal it causes neurotransmitters to be released into the synaptic cleft. The neurotransmitters then bind with special "postsynaptic receptors" in the dendrites of the receiving neuron. \n\nWhen a postsynaptic receptor receives a neurotransmitter it can either cause a nerve impulse to travel down the neuron or it can inhibit a nerve impulse depending on the neurotransmitter released. \n\nNeurotransmitters which propagate nerve impulses in the receiving neuron are called excitatory neurotransmitters. Those which inhibit nerve impulses are called inhibitory neurotransmitters. \n\nNeurotransmitters are sythesized in the cell body (the soma) and migrate down the axon to the presynaptic terminals. Here they are stored in little packets called vesicles which fuse with the synaptic membrane. When a depolarizing current (the action potential) is received, these vesicles release their contents into the synaptic cleft. \n\nNeurotransmitters activate receptors by "sticking" to them and thus preventing other neurotransmitters from activating them. Inactivation of the transmitter happens in one of three ways: \n\n\nReabsorption of the neurotransmitter into the neuron. This is known as reuptake. \n\nDestruction of the neurotransmitter with special chemicals called enzymes. This is known as enzymatic degradation. \n\nBy the neurotransmitter becoming deteched from the receptor and drifting out of the synaptic cleft. This is known as diffusion.\nSubstances that effect neurotransmission but are not neurotransmitters can be broadly divided into two categories - agonists and antagonists. \n\nAgonists make transmission of nerve impulses more likely. They do this in a number of ways including preventing reuptake (cocaine works this way). \n\nActually triggering the receptor themselves (nicotine works this way) \n\nAnd by making the receptor more responsive (a lot of anti-anxiety drugs work like this). \n\nAntagonists do the opposite - they interfere with nerve transmission across the synapse sometimes by blocking receptor sites (many spider and snake venoms work this way) \n\nAnd sometimes by preventing release of the neurotransmitter from the presynaptic terminal (many anti-psychotic drugs operate like this). \n\nThe following is an partial list of neurotransmitters, together with the sites in which they work: \n\nNeurotransmitters Group Neurotransmitter Region of Operation \nAcetylcholine Acetylcholine Central Nervous System (CNS), Peripheral Nervous System (PNS) and Autonomic Nervous System (ANS)  \nSerotonin SerotoninCNS and PNS \nAmino acids Glutamate, GammaAminobutyric Acid (GABA), Glycine, Aspartate  CNS \nHistamine Histamine Hypothalamus \nCatecholamines Norpinephrine, Epinephrine (Adrenalin) CNS and Sympathetic Nervous System \nNeuropeptides Endorphins (Enkephalins and Dynorphins), Substance P CNS \nDopamine Dopamine CNS \nNucleotides Adenosine, Adenosine Triphosphate (ATP) CNS, PNS and ANS \nNitric oxide Nitric oxide CNS
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The parasympathetic nervous system is antagonistic to the sympathetic nervous system. It's not that one tries to be active all the time, they work together and one is more active than the other in certain types of situations. \n\nThe parasympathetic system does the following:\n\nHeart - slows it down\npupils - constricts them\nlungs - constricts airways\nstomach - stimulates digestion\nintestines - dilates blood vesssels so that more blood can go to the intestines\nbladder - stimulates it\ngenitals - stimulates erection
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It is basically a drug that depresses the central nervous system (CNS), which causes calmness, relaxation, reduction of anxiety, sleepiness, slowed breathing, slurred speech, staggering gait, poor judgment, and slow, uncertain reflexes.
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norepinephrine and mescaline are spelled correctly. Here is some more information about these molecules.\n\nmescaline- http://en.wikipedia.org/wiki/Mescaline\nnorepinephrine- http://en.wikipedia.org/wiki/Norepinephrine
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Methamphetamines in general mimick the neurotransmitters Epinephrine and Norepinephrine. These are naturally produced in the body and regulated by other neurotransmitters. The meth will bind to the receptors for those neurotransmitters resulting in a stimulant effect of high magnitude. The more you use the drug the more tolerant the body becomes and the less natural epinephrine and norepinephrine are produced by the body to compensate for the excess(as it recognizes the drug as the neurotransmitter and will quit producing it over time). This results in a higher threshold to get "high" and therefore more of the drug required. At the same time the body is become dependant on the artificial supply being given to the body and the user becomes physically as well as psychologically dependant. The drug itself is extremely corrosive causing widespread damage to any and all tissue it comes in contact with, ultimately resulting in perferated septum, rotting teeth and gums, erroding esophagus, failing kidneys, etc, etc, etc. Dependant users get to the point that they will give up anything to get the drug, ultimately costing them their jobs, their relationships, their dignity and their life.
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My recollection is that muscarinic receptors cause vasodilation.  This is supported by the resource below: \n  \n"ACh on Blood flow: \n\nA very tricky question.  The only place one finds muscarinic receptors on blood vessels is in some of them supplying skeletal muscles.  In this case, ACh is released from sympathetic nerves.  Following our "Fight or Flight" scenario, we can predict that ACh will dilate these vessels.  However, if we give an i.v. dose of ACh, heart rate will go down (parasympathetic action) and this may decrease blood flow in the total system. \n"
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Clonidine is an antihypertensive.  It lowers your blood pressure.\nSide Effects:\nDifficulty in breathing, dizziness (extreme) or faintness,  feeling cold,  pinpoint pupils of eyes,  slow heartbeat,  unusual tiredness or weakness (extreme), most commonly itchiness of the skin
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I looked it up. It sounds like Phentermine.\nPhentermine is a sympathomimetic amine, which is similar to an amphetamine. It is also known as an "anorectic" or "anorexigenic" drug. Phentermine stimulates the central nervous system (nerves and brain), which increases your heart rate and blood pressure and decreases your appetite.\n\nPhentermine is used as a short-term supplement to diet and exercise in the treatment of obesity.\n\nPhentermine may also be used for purposes other than those listed in this medication guide.
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Adrenaline is released into the blood stream.  Another name for Adrenaline is Epinephrine.\n\nEpinephrine plays a central role in the short-term stress reaction—the physiological response to threatening or exciting conditions. It is secreted by the adrenal medulla. When released into the bloodstream, epinephrine binds to multiple receptors and has numerous effects throughout the body. It increases heart rate and stroke volume, dilates the pupils, and constricts arterioles in the skin and gut while dilating arterioles in leg muscles. It elevates the blood sugar level by increasing hydrolysis of glycogen to glucose in the liver, and at the same time begins the breakdown of lipids in fat cells.
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The sympathetic nervous system, when highly activated, causes stress-induced responses during times of danger.  So anything that aids skeletal muscle efficiency and motion will be stimulated.  So, blood flow will be directed towards skeletal muscle, nervous tissue, and brain, and away from everything else.  In addition to blood flow, all other systems will be inhibited (you dont want the intestines, stomach, kidneys, etc working hard while not getting enough blood flow).  So, the digestive systems and everything else will be inhibited.  If your sympathetic system is very highly stimulated, for an extended period of time, you will often get nauseous enough to vomit-because food will have been sitting in your stomach without being digested.  It may also cause diarrhea or constipation because of lack of digestive activity.\nGood luck in your classes.
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Adrenaline (epinephrine) causes the pupil to dilate and the upper eyelid to raise a little bit more.  This is considered an evolutionary benefit in the "fight or flight" phenomenon as it helps seeing while you are fighting/running.
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GENERIC NAME: nortriptyline\nBRAND NAME: Pamelor, Aventyl\nDRUG CLASS AND MECHANISM: Nortriptyline is an antidepressant medication of the tricyclic class. Medications in this class are often referred to as tricyclic antidepressants, or TCAs. Depression is an all-pervasive sense of sadness and gloom. In some patients with depression, abnormal levels of brain neurotransmitters (chemicals that the nerve cells use to communicate with each other) may be responsible for the depression. Nortriptyline elevates the mood ("anti-depresses") by raising the level of neurotransmitters in brain tissue.\n\nPRESCRIPTION: yes\n\nGENERIC AVAILABLE: yes\n\nPREPARATIONS: Capsules: 10mg, 25mg, 50mg, 75mg.\n\nSTORAGE: Nortriptyline should be stored below 86°F (30°C) in a tight, light resistant container.\n\nPRESCRIBED FOR: Nortriptyline is used to elevate the mood of patients with depression. Nortriptyline is also a sedative and is useful in depressed patients with insomnia, restlessness, and nervousness. It also has been found to be helpful for treating chronic pain and the pain of neuralgia.\n\nDOSING: The dose of nortriptyline is tailored to the patient's needs. Sometimes, physicians will start with relatively low doses, such as 25mg, given three times a day, to reduce the risk of excessive sedation early in the course of therapy; doses then will be increased slowly upwards. It may take several weeks after starting to take nortriptyline until the full effects of a dose to be seen. Other physicians prefer to give nortriptyline once daily, in which case it is generally given at bedtime to take advantage of its sedating properties. Elderly persons and patients with advanced liver disease may need lower doses.\n\nDRUG INTERACTIONS: Nortriptyline exaggerates the effects of other medications and drugs that slow the brain's processes, such as alcohol, barbiturates, benzodiazepines (e.g. lorazepam, Ativan), and narcotics. Reserpine, given to patients taking TCAs, can have a stimulatory effect. Nortriptyline and other TCAs should not be used with monoamine oxidase inhibiting drugs, for example, isocarboxazid (Marplan), phenelzine (Nardil), tranylcypromine (Parnate), and procarbazine (Matulane). High fever, convulsions and even death can occur when these drugs are used together.\n\nCimetidine (Tagamet) can increase nortriptyline blood levels and possibly cause side effects. Other drugs which share this effect include propafenone (Rythmol), flecainide (Tonocard), quinidine (Quinidex, Quinaglute), and fluoxetine (Prozac).\n\nPREGNANCY: There is very little information about the effects on the fetus of nortriptyline given to pregnant women. Physicians may elect to use it if its benefits are deemed to outweigh potential risks.\n\nNURSING MOTHERS: It is not known if nortriptyline is secreted in breast milk.\n\nSIDE EFFECTS: The most commonly encountered side effects associated with nortriptyline include fast heart rate, blurred vision, urinary retention, dry mouth, constipation, weight gain or loss, and low blood pressure on standing. Rash, hives, seizures, and hepatitis are rare side effects. Nortriptyline also can cause elevated pressure in the eyes of some patients with glaucoma. Overdose with nortriptyline can cause life-threatening abnormal heart rhythms or seizures
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It increases the neuronal firings in the areas the stimulant affects. It makes your central nervous system work more.
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Adreniline. It's a vasoconstrictor, reducing bloodflow in times of excitement or pain \n\nI'd see a doctor.  You might have a neurological disorder.
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Nervous system is much faster in their rate of control mostly because of the way they communicate.  Nervous system communicates via neurotransmitters that are sent from one neuron to the next at a synapse.  This neurotransmitter, such as acetylcholine, will cause ion channels to open and an action potential to take place.  The rate at which these action potentials take place determines the action or sense that your nervous system transmits.  The endocrine system, on the other hand is a lot slower because the hormone molecules it sends out have to find its way to the effector organs.  To do this, the hormones have to travel through the blood system, reach the organs, and then bind to the cellular receptors.  Even after this has happened, these endocrine hormones tend to cause cascades in target cells to take place before the initended effect takes place.  These cascades include tyrosine kinase or g-protein coupled receptor phosphorylation cascades that ultimately result in transcription and translation of genes.  This process also is a lot slower than the process of action potential in the nervous system.