what is the effect of a named agonist and a named antagonist on a receptor transduction mechanism?
484436
Without knowing the names, I can tell you what an agonist and antagonist do in general, in receptor-mediated signal transduction.  An agonist acts to mimic the natural ligand, so it activated the receptor transduction system.  An antagonist is the opposite-it binds the receptor and inhibits the signal transduction system.
122144
go to www.webmd.com and type the name in the search box. It will give you all the information you need including side effects interactions mostly everything on the medicine that you want to know.
967758
It is called Phosphorylation\n\nIn eukaryotes, protein phosphorylation is probably the most important regulatory event. Many enzymes and receptors are switched "on" or "off" by phosphorylation and dephosphorylation. Phosphorylation is catalyzed by various specific protein kinases, whereas phosphatases dephosphorylate.\n\nA protein kinase is an enzyme that modifies other proteins by chemically adding phosphate groups to them (phosphorylation). This usually results in a functional change of the target protein (substrate) by changing enzyme activity, cellular location, or association with other proteins. Up to 30% of all proteins may be modified by kinase activity, and kinases are known to regulate the majority of cellular pathways, especially those involved in signal transduction, the transmission of signals within the cell. The human genome contains about 500 protein kinase genes; they constitute about 2% of all eukaryotic genes.\n\nAdding a phosphoryl (PO3) to a polar R group of an amino acid might not seem like it would do much to a protein, but it can actually turn a nonpolar hydrophobic protein into a polar and extremely hydrophilic molecule. Phosphorylation is observed on serine, threonine, tyrosine and histidine residues.\n\nAn example of the important role that phosphorylation plays is the p53 tumor suppressor gene, which—when active—stimulates transcription of genes that suppress the cell cycle, even to the extent that it undergoes apoptosis. However, this activity should be limited to situations where the cell is damaged or physiology is disturbed. To this end, the p53 protein is extensively regulated. In fact, p53 contains more than 18 different phosphorylation sites.
579789
I think you actually mean tetrodotoxin.  It's a neurotoxin that binds the pores of sodium channels, thus inhibiting potentiaion.  If the toxin is ingested (usually happens by accidental ingestion of certain fish) it can cause paralysis of the individual's diaphragm followed by death due to respiratory failure (i.e. you suffocate).
237583
for skeletal muscle - nerve impulse depolarises muscle cell surface, calcium released, ATP driven actin-myosin contraction cycle.
942751
Sorry for my previous answer, I was mistaken. \nI believe answer is B. A is correct, but I don't think it is why it affect target tissue for loger time. I don't think C is correct, but it could be. D is certainly wrong and E too. I haven't seen this in a while. Sorry I couldn't be more help.
69908
Many (perhaps most) cells  stop growing when the reach confluence (this is called "Contact inhibition"). Generally, they do not die when they hit confluence, but certainly it will change the way they react to drug treatment and could be relevant.
512703
Neurotransmitters transmit impulse from one neuron to the other neuron.It's effect local. On the other hand, neuromodulators have hormone-like effect which can circulate in the bloodstream.For example:Nerve growth factor(NGF)
801326
Signal molecules are often called ligands, and they bind to receptors on the outside of cells.  The proteins (or glycoproteins) that we call receptors are membrane bound proteins (like a G-protein coupled receptor.  So, ligands (like a hormone) bind reversibly to these receptors, and begin the G-Protein signaling cascade.  After stimulating the receptor, they are simply knocked off or fall off.\n\nWhen a ligand stimulates a G-Protein coupled receptor, the receptor changes conformation, allowing it to associate with a 3-unit (trimeric) G-Protein.  The alpha unit of the G-protein interacts with the receptor, and changes, where a bound GDP is replaced by a GTP molecule.  The G-protein/GTP complex then activates a protein called adenylyl cyclase, which converts free cytoplasmic ATP into cAMP (cyclic AMP).  The cAMP then activates PROTEIN KINASES, which in turn activate transcription factors, initiating transcription of some final gene product.\n\nLet me give you an example.  Fight or flight response, the body needs extra glucose to give to muscle cells, the heart, the brain, etc . . . the sympathetic system is activated, and the adrenal gland releases epinephrine.  Epi then circulates where in liver cells, it binds to a G-Protein coupled receptor called a Beta-adrenergic receptor (adrenergic always refers to a receptor that epinephrine binds to).  The receptor interacts with a G-Protein, the G-protein complexes with GTP, the GTP/G-protein complex activate adenylyl cyclase, ATP is converted to cAMP, transcription factors are activated, proteins that lead to glucose production are transcribed and translated.  As a result, more glucose is released into the bloodstream for skeletal muscle to use as energy.\n\nThis is just one example of how a G-Protein works, there are others, but this gives you a basic idea of cell signaling.  Cell signaling is EVERYWHERE, it is very important to understand it.
700278
It's effects!\n\nBeta blockers block the action of endogenous catecholamines, epinephrine (adrenaline) and norepinephrine (noradrenaline) in particular, on β-adrenergic receptors, part of the sympathetic nervous system which mediates the "fight or flight" response.\n\nThere are three known types of beta receptor, designated β1, β2 and β3. β1-Adrenergic receptors are located mainly in the heart, kidney, and adipose tissue. β2-Adrenergic receptors are located mainly in the heart, lung, GI tract, liver, pancreas, and skeletal muscle. The role and location of β3-receptors is less well-defined.\n\n\n β-Receptor antagonism\nStimulation of β1 receptors by epinephrine induces a positive chronotropic and inotropic effect on the heart and increases cardiac conduction velocity and automaticity. Stimulation of β2 receptors induces smooth muscle relaxation (resulting in vasodilation and bronchodilation amongst other actions), induces tremor in skeletal muscle, increases glycogenolysis in the liver and skeletal muscle.\n\nBeta blockers inhibit these normal epinephrine-mediated sympathetic actions, but have minimal effect on resting subjects. That is, they reduce the effect of excitement/physical exertion on heart rate and force of contraction, dilation of blood vessels, opening of bronchi, reduce tremor, and breakdown of glycogen.\n\nIt is therefore somewhat unexpected that non-selective beta blockers have an antihypertensive effect, since they appear to cause vasoconstriction. The antihypertensive mechanism appears to involve: reduction in cardiac output (due to negative chronotropic and inotropic effects), reduction in renin release from the kidneys, and a central nervous system effect to reduce sympathetic activity.\n\nAntianginal effects result from negative chronotropic and inotropic effects, which decrease cardiac workload and oxygen demand.\n\nThe antiarrhythmic effects of beta blockers arise from sympathetic nervous system blockade – resulting in depression of sinus node function and atrioventricular node conduction, and prolonged atrial refractory periods. Sotalol, in particular, has additional antiarrhythmic properties and prolongs action potential duration through potassium channel blockade.\n\n\nIntrinsic sympathomimetic activity\nSome beta blockers (e.g. oxprenolol and pindolol) exhibit intrinsic sympathomimetic activity (ISA). These agents are capable of exerting low level agonist activity at the β-adrenergic receptor while simultaneously acting as a receptor site antagonist. These agents, therefore, may be useful in individuals exhibiting excessive bradycardia with sustained beta blocker therapy.\n\nAgents with ISA are not used post-myocardial infarction as they have not been demonstrated to be beneficial. They may also be less effective than other beta blockers in the management of angina and tachyarrhythmia (Rossi, 2006).\n\n\nα1-Receptor antagonism\nSome beta blockers (e.g. labetalol and carvedilol) exhibit mixed antagonism of both β- and α1-adrenergic receptors, which provides additional arteriolar vasodilating action.\n\n\n Other effects\nBeta blockers decrease nocturnal melatonin release, perhaps partly accounting for sleep disturbance caused by some agents (Stoschitzky et al., 1999).
259748
Pharmaceutically bronchodilators belong to β-2 mimetics - they act on β-2 receptors in bronchial smooth muscle and bronchial mucous membranes. Bronchodilators, particularly non-prescription ones, are often misused as stimulants. A common side-effect of these medications is desensitization, which may produce refractory bronchospasm.\nBrand names of common bronchodilators :\n\n    * Ventolin (salbutamol)\n    * Primatene (epinephrine)\n    * Flixotide\n    * Serevent\n    * Accu-Hale\n\nThese medications open the airways.\n\nI am anaphylactic, which means that I need to inject epinephrine in order to keep my airway from closing - which happens if I get stung by a bee.
670939
No, that's not right.  The movement of sodium and potassium across the membrane carries the action potential along the neurite, but not between neurons.  Neurotransmitters-released by one neurons (usually at an axon terminal) crosses the synapse, and binds with specific receptors (usually on the dendrite or axon hillock). Once it binds, it usually opens ligand-gated sodium channels.  \n\nYou asked the name of the chemical, but it's actually a class of chemicals, not one, called neurotransmitters.  Common ones are glutamate, acetylcholine, seretonin, epinephrine and dopamine, but there are literally dozens of them.
811688
I would have to guess that it involves the neutralization reaction of more than 2 substances.\n\nJust a guess
292429
Proteins can not penetrate plasma membranes\nCyclic AMP (mediates neurotransmitters)\nHormone (first messenger) binds to receptor\nReceptor binds G-protein\nG-protein binds GTP, releasing GDP (has GTPase)\nActivated G-protein moves along membrane binds to Adenalyte cyclase,\nhydrolyzes it’s bound GTP to GDP.\ncAMP generated from ATP (secondary messenger)\nCyclic AMP (cAMP) diffuses throughout cell, triggering protein kinases\n(enzymes)\nExample: Epinephrine (adrenaline) on fat cell-break down glycogen and fat.\nPhosphodiesterase (intercellular enzyme) degrades cAMP\nImplications\nMultiplier effect: 1 Adenylate cyclase: ?? cAMP\nKinase catalyzes hundreds of reactions\nSingle hormone may catalyze millions of product molecules\nSequence regulated by:\nTarget cell type, specific protein kinases, and the initiating hormone\nSecondary messenger system: The PIP-Calcium signal mechanism\nSome hormones (e.g. epinephrine) mediated by Calcium, not cAMP.\nHormone binds to receptor\nG protein activated as GTP binds, displacing GDP\nG protein binds to and activates a membrane bound phospholipase, and\ninactivates\nPhospholipase splits PIP2 into IP3 and diacylglycerol (secondary messengers)\nPIP2 : phosphatidyl inositol biphosphate; IP3: inositol triphosphate\nIP3: Calcium from ER (endoplasmic reticulum)\nDiacylglycerol: Protein kinases\nCa2+: alters plasma membrane ion channels and also binds to Calmodulin, which\namplifies cellular response (decreases the energy of activation)\n\nalso see:
479
There are at least 3 types of beta receptors in the body - beta 1, 2, and 3 - and they are sensitive to epinephrine and norepinephrine. beta 1 controls heart rate and force of contraction in the heart (an increase in these will increase blood pressure, thus blocking them will lower blood pressure). beta 2 controls smooth muscle many places in the body. beta 3 receptors have less well defined role in fat metabolism.\n\nThe late American scientist Raymond Ahlqvist suggested already in 1948 that opposite effects of catecholamines were mediated by different receptors in the target organs, which he called alpha- and beta-receptors. http://nobelprize.org/medicine/laureates/1988/press.html
686729
By chemically blocking pain receptors
436441
Because the drug binds to it. When the drug binds to the receptor, the drug begins to work.