acetylecholine and atropine mechanism?
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The chemical compound acetylcholine, often abbreviated as ACh, was the first neurotransmitter to be identified. It is a chemical transmitter in both the peripheral nervous system (PNS) and central nervous system (CNS) in many organisms including humans.\n\nAtropine is a tropane alkaloid extracted from the deadly nightshade (Atropa belladonna) and other plants of the family Solanaceae. It is a secondary metabolite of these plants and serves as a drug with a wide variety of effects. Being potentially deadly, it derives its name from Atropos, one of the three Fates who, according to Greek mythology, chose how a person was to die.\n\n\n\nGenerally, atropine lowers the "rest and digest" activity of all muscles and glands regulated by the parasympathetic nervous system. This occurs because atropine is a competitive antagonist of the muscarinic acetylcholine receptors. (Acetylcholine is the neurotransmitter used by the parasympathetic nervous system.) Therefore, it may cause swallowing difficulties and reduced secretions.\nOphthalmic use\nTopical atropine is used as a cycloplegic, to temporarily paralyze accommodation, and as a mydriatic, to dilate the pupils. Atropine degrades slowly, typically wearing off in 2 to 3 days, so tropicamide is generally preferred as a mydriatic. In atropine-induced mydriasis, the mechanism of action involves blocking the contraction of the circular pupillary sphincter muscle (which is normally stimulated by acetylcholine release), thereby allowing the radial pupillary dilator muscle to contract and dilate the pupil. Atropine is contraindicated in patients predisposed to narrow angle glaucoma.\n\n[edit]\nResuscitation\nInjections of atropine are used in the treatment of bradycardia (an extremely low heart rate), asystole and pulseless electrical activity (PEA) in cardiac arrest. This works because the main action of the vagus nerve of the parasympathetic system on the heart is to slow it down. Atropine blocks that action and therefore may speed up the heart rate.\n\nThe main action of the parasympathetic nervous system is to stimulate the M2 muscarinic receptor in the heart, but atropine inhibits this action.\n\n[edit]\nSecretions and brochoconstriction\nAtropine's actions on the parasympathetic nervous system inhibits salivary, sweat, and mucus glands. This can be useful in treating Hyperhidrosis and can prevent the death rattle of dying patients, even though it has not been officially indicated for either of these purposes.\n\n[edit]\nAntidote for organophosphate poisoning\nBy blocking the action of acetylcholine at muscarinic receptors, atropine also serves as an antidote for poisoning by organophosphate insecticides and nerve gases. Troops who are likely to be attacked with chemical weapons often carry autoinjectors with atropine and obidoxime which can be quickly injected into the thigh. It is often used in conjuntion with Pralidoxime chloride.\n\nSome of the nerve gases attack and destroy acetylcholinesterase, so the action of acetylcholine becomes prolonged. Therefore, atropine can be used to reduce the effect of ACh.\n\n[edit]\nSide effects and overdoses\nAdverse reactions to atropine include ventricular fibrillation, supraventricular or ventricular tachycardia, giddiness, nausea, blurred vision, loss of balance, dilated pupils, photophobia, and possibly, notably in the elderly, confusion, hallucinations and excitation. These latter effects are due to the fact that atropine is able to cross the blood-brain barrier. Because of the hallucinogenic properties, some have used the drug recreationally, though this is very dangerous.\n\nIn overdoses, atropine is poisonous. Atropine is sometimes added to other potentially addictive drugs; abuse of those drugs is then prevented by the unpleasant effects of atropine overdose.\n\nAtropine can cause heart rate slowing when given at very low doses, presumably as a result of a weak partial agonist effect at the cardiac muscarinic receptors.\n\n\nT
350260
Abnormally low levels of acetycholine have been observed in the brains of people with Alzheimer's disease.
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GHB got a bum rap.  it's just more nonsense hysteria to justify the bloated budgets of the police state.\n\nThat aside, you don't convert beta to gamma.  suggesting an elimination failed to consider that the double bond formed will be more stable in conjugation with the carbonyl group; you'll get crotonic acid.  Subsequent hydrolysis would give you a mixture of alpha and beta.\n\nyou'd have much better luck trying to figure out a way to do it starting with GABA.\n\nOf course, if you have to ask, you lack the skilz.
391224
There are two classes of acetylcholine receptors, muscarinic and nicotinic (see Molecular Biology, Pharmacology, and Brain Distribution of Subtypes of the Muscarinic Receptor). These receptors play major roles in the function of the body. In brain, evidence suggests a role for muscarinic receptors in memory function (28, 71) and in the pathophysiology of affective illness (46, 47, 79) and schizophrenia (24, 50, 85, 86). Because of their putative role in cognitive function, muscarinic receptors have been a focus of research in Alzheimer's disease (see Experimental Therapeutics).\n\nResearchers defined the two classes of cholinergic receptors early in this century on the basis of tissue responses to certain agonists and antagonists (22). A response caused by muscarine, an alkaloid derived from a poisonous mushroom (Amanita muscaria), and antagonism of a response caused by atropine, an alkaloid from the deadly nightshade (Atropa belladonna—a favorite of poisoners in past centuries), defined muscarinic receptors in a tissue. On the other hand, response to nicotine and blockade by d-tubocurarine (one of the alkaloids from the South American arrow poisons) defined nicotinic receptors. These definitions for the two types of cholinergic receptors are still used today.\n\nMuscarinic receptors are widely distributed throughout the body. They mediate various types of responses in many different tissues—such as cardiac tissue, smooth muscle, and exocrine glands—and in cells throughout the peripheral and central nervous system. Within the nervous system, muscarinic receptors are present on some axon endings (heteroreceptors and autoreceptors), regulating neurotransmitter release (1, 67, 68, 90). These receptors are also on the soma and dendrites of many types of neurons, including cholinergic and noncholinergic neurons (67, 95).\n\nIn the past several years, discoveries by molecular biologists have made the field of muscarinic receptors immensely interesting and complex. At a time when pharmacologists could identify at most three subtypes of muscarinic receptors, molecular biologists showed that at least five different muscarinic receptors exist on the basis of molecular cloning experiments (15, 16, 54, 55, 63). Much knowledge about these receptors has come from the use of transfected cell lines that have incorporated into their genome and express the gene encoding the specific muscarinic receptor.\n\nThis chapter will focus mainly on the biochemical events associated with activation of muscarinic receptors. The concepts of receptors, their effectors, and second messengers will be presented along with a general discussion of the types of membrane-bound receptors. Specific aspects of transduction at cholinergic receptors will be presented along with a brief discussion of the neuropsychopharmacology of muscarinic receptors.\n\nRECEPTORS\n\nThe concept of a receptor was put forth in the latter part of the nineteenth century and the early part of this century by Professors J. N. Langley and Paul Ehrlich. Professor Ehrlich has stated "the toxin must unite . . . with `receptors' in order for the toxin to have its effects" (30). Professor Langley used the term "receptive substance" (56).\n\nA receptor is a highly specialized protein, which, in most cases, is a transmembrane spanning protein on the cellular surface (receptors for steroid hormones are intracellular). This receptor protein has the unique ability to recognize (bind) specific molecules. All neurotransmitters, neuromodulators, and hormones have specific receptors. Many neurotransmitters are known to have more than one type of receptor to which they bind.\n\nCurrently, receptors may be classified into four groups based upon their signal transduction mechanisms: (i) receptors that are ligand-gated ion channels [e.g., the nicotinic acetylcholine (21, 65) and gamma-aminobutyric acid (GABA) receptors (13, 75)]; (ii) receptors that are enzymes [e.g., the ins
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Breathing is normally autonomic, but we do have control over it when we think about it.  This makes it somewhat unique in the autonomic nervous system.  \n\nIf I take two Vicodan, it knocks out the autonomic part of the system and I have to think about breathing.  That's really fun.  /sarcasm
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Hi there !\nWhat do you mean by the question ? \nYou expect somebody to describe the "entire digestion" and the "metabolism mechanism" of the Human body in this column ?\nBetter verify the "Book of Physiology by Guyton" or "Chatterjee"..they have given beautiful descriptions ! \nbest wishes !
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My sister gets migranes and uses Dramamine (for motion sickness) and Ibuprophen. She says the combination works like magic.
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It causes migranes yet it continues to be used as a tastemaker. The molecular structure may induce certain changes in conformation of invivo proteins/ their expressio, and vasodilation/constriction of blood vessels in the head, casuing the migraine.
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1- No. Because there is no NETO FLOW of chloride ions. Chloride ions can pass membrane. There is active pump that expels them out from the cell. But they get into the cell by passive diffusion, so they are in constant extracellular/intracellular equilibrium and don't affect resting membrane potential.\n\n2- "Excitable cells (nerves, muscles) have higher membrane potentials than non excitable cells (red blood cells, fibroblasts, etc.)"\n3- Absolute refractory period seems to be somewhat longer than relative. See link: http://www.unmc.edu/Physiology/Mann/mann3b.html\n4- Curare is a mixture of plant toxins. South American Indians use it on tips of their arrows to paralyze the pray. Purified active component of that poison is d-tubocurarine, which blocks signalization through neuromuscular synapse because it binds to nAChR - and so it blocks binding of ACh.
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Oxymetazoline works on the adrenergic alpha receptors, and therefore it will have no direct effect on the lungs because they have adrenergic beta receptors.  \nOxymetazoline is an active ingredient in Afrin.  Is that what you mean?  Do not use the Afrin spray for an extended period of time without contacting your doctor.\nAn inhaler may not be the best choice to stop a cough.  Very few OTCs really help stop coughs.
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take a carboxylic acid and couple under normal conditions with an O-alkylated/acylated hydroxylamine.\n\nBy normal conditions, I mean normal peptide coupling conditions usined EDC, DIC/HOBt, CDI, PyBOP, PyBrOP, TBTU etc etc etc
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A lot of questions. First cigarette smoke contains nicotine and Carbon monoxide and tear and further for the body toxic ingredients, which have following effect. Nicotine increases the vascular tension of small arteries, which causes the bloodpressure to rise. There may ba also a transient increase in respiratory rate through a centrally stimulating effect. If a patient has a rapid respiratory rate, it can be caused by insufficient gas exchange through in the lung. The effectiveness of the lungs gas exchange gets worse, through longterm smoking exposure. tear and toxic ingredients seize the function of the microvilli, which are little mobile hairlike formations on the surface of bronchial cells. Their job is to transport little foreign bodies and mucus etc. out of the lung. Small areas of the lung are being plugged up and are getting inflamed. The person developes chronic bronchitis with a decrease of normally functioning lung tissue. Also Atelectasis may develop. \nThere are many reasons, why bloddpressure rises. Smoking is one of them, often it is not clear if smoking or other causes i.e. genetic predeterminatiion are contributing to high blood pressure.\nSecond the blood pressure measured is the pressure created by the left heart. If right heart pressure rises, that means thge left heart is unable to transport enough blood away form the right heart outflow, which can cause eventually pulmonary hypertension or high bloodpressure in the pulmonary arteries (the one going away from the right heart). That happens, when the left heart does not work right.\nFor smokers the blood pressure is normally only high in the left heart outflow system.\nPlasma flow is widely independent from blood systolic  pressure alone. To assess plasma flow, the osmotic venous pressures also need to be known.\nThe body usually tries to maintain homeostasis.\nThat means acutely (when the bloodpressure goes up suddenly) ANP counteracts that development and ANP goes up. Chronically elevated BP would probably not change the ANP Level. Accordingly with Aldosterone. That means the Aldosterone level would go down with sudden elevated BP
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Hi. \nI just did a Google Search for ataxia.\nBTW, if you search for attaxia you will get the wrong answers.  No offense, just trying to help.\nI am sending the link that hopefully you will check out under "sources".  There are alot of different ataxia sites that might give you some encouragement.\nI Care!\n~Linda S~\naka ~longleggedblonde1378~
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The three answers above me only give you half of the answer.  There are muscarinic and choloinergic acetylcholine (Ache) receptors in the body.  \n\nI could give you what I know about Ach, but here is a complete list from wikipedia.com.  I even learned a few things about Ach from this information, and I have a PhD in neuroscience.\n\nAcetylcholine is released by:\n\nCNS neurons arising from 3 key areas:\n\nDorsolateral pons, which have broad targets through the brain, and are involved in REM sleep \n\nBasal Forebrain, the major source of cholinergic innervation throughout the cortex, implicated in the facilitation of learning \n\nmedial septum, which projects largely to the limbic system, and may induce rhythmic firing in the hippocampus critical to learning \n\nmany interneurons of the basal ganglia are also cholinergic \nsome PNS neurons, including \n\nmotor neurons (of the somatic nervous system), causing muscle contraction of striated muscle \n\nthe autonomic nervous system: \n\npre- and post-ganglionic parasympathetic neurons \n\npreganglionic sympathetic neurons (and also postganglionic pseudomotor neurons, i.e., the ones that control sweating) \n\nHope this is what you need.
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http://pubs.acs.org/cgi-bin/abstract.cgi/jafcau/1953/1/i03/f-pdf/f_jf60003a008.pdf?sessid=6006l3
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My sister used to do that.  She ended up having athsma.  Go to the doctor ASAP
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Major component is TAURIN... \n\nIt is amino-acid taht exists in human body but in some condition level of it is going up (normally in parallel with adrinalin)... AND IT IS WAIKING YOU UP...\n\nBut, human body is simple, if that was forcing of power using then will be hard time in next time... Long time useing of touring can affect not only brain but destabilize all of organism...\n\nB-group vitamins are compensating (have to be) the demage by touring... BUT it is not so right an depends of body conditions...\n\nIf you will mix it with alchogole - it is the best way to fly a way and... BE DIE...\n\nJust take it in critical situation... it is not 'by-the-way-drink'...