• These synaptic vesicles contain acetylcholine, which is released into the synaptic cleft and stimulates the acetylcholine receptors on the muscle. (wikipedia.org)
  • Activation of sigma receptors inhibits the release of acetylcholine (ACh) from guinea pig ileum myenteric plexus preparations. (aspetjournals.org)
  • They accomplish this by two mechanisms: histamine released by ECL cells in the stomach is blocked from binding on parietal cell H 2 receptors which stimulate acid secretion, and other substances that promote acid secretion (such as gastrin and acetylcholine ) have a reduced effect on parietal cells when the H 2 receptors are blocked. (wikidoc.org)
  • Gastrin (G) cells release gastrin, which works on CCK 2 receptors on ECL cells. (drugbank.com)
  • Upon release, histamine acts on H 2 receptors expressed on the basolateral membrane of parietal cells, leading to increased intracellular cAMP levels and activated proton pumps on parietal cells. (drugbank.com)
  • Proton pump releases more protons into the stomach, thereby increasing the secretion of acid. (drugbank.com)
  • However, because presynaptic stores of ACh and the postsynaptic response to ACh remain intact, rapid repetitive stimulation or voluntary activation that aids in the release of quanta will raise the endplate potential above threshold and permit generation of muscle action potential. (medscape.com)
  • In LEMS, antibodies against VGCC, particularly the P/Q-type VGCC, decrease the amount of calcium that can enter the nerve ending, hence less acetylcholine can be released from the neuromuscular junction. (wikipedia.org)
  • Lambert-Eaton myasthenic syndrome (LEMS) is a rare presynaptic disorder of neuromuscular transmission in which quantal release of acetylcholine (ACh) is impaired, causing a unique set of clinical characteristics, which include proximal muscle weakness, depressed tendon reflexes, posttetanic potentiation, and autonomic changes. (medscape.com)
  • Physiologic studies of neuromuscular transmission demonstrate that ACh release from the motor nerve terminal is impaired in the LEMS muscle. (medscape.com)
  • The number of quanta released by a nerve impulse is diminished. (medscape.com)
  • These symptoms may arise from release of cytokines involved in the inflammatory or immune response or from mediators involved in tumor cell death, such as tumor necrosis factor-alpha. (msdmanuals.com)
  • It was proposed that the toxicity arose from the thiourea group, and similar guanidine -analogues were investigated until the ultimate discovery of Cimetidine (common brand name Tagamet). (wikidoc.org)
  • Similar doses significantly ( 0.05) decreased the release of proteins like TNF-, IL-1, and iNOS in the brain tissue. (health-e-nc.org)
  • This assumption is supported by read-across data from an acute toxicity study by inhalation route with Guanidine Hydrochloride, were systemic effects were observed. (europa.eu)
  • Guanidine hydrochloride is used as pharmaceutical. (europa.eu)
  • Chemically, guanidine (aminomethanamidine) hydrochloride is a crystalline powder freely soluble in water and alcohol. (nih.gov)
  • Each tablet contains 125 mg of guanidine hydrochloride with no color additive in the base. (nih.gov)
  • Safe use of guanidine hydrochloride in pregnancy has not been established. (nih.gov)
  • So it makes me wonder if Guanidine hydrochloride has been attempted to treat CJD in humans. (substack.com)
  • This is accomplished by increasing the concentration of acetylcholine at cholinergic synapses through reversible inhibition of its hydrolysis by acetylcholinesterase. (illumina.com)
  • This inhibits the hydrolysis of acetylcholine released from functioning cholinergic neurons, thus leading to an accumulation of acetylcholine at cholinergic synapses. (illumina.com)
  • The aim of the project is to determine how disruption of cholinergic activation of striatal GABAergic interneurons alters striatal signalling and striatum-based behaviour by using a mouse model with deletion of the β2 nicotinic acetylcholine receptor subunit in striatal GABAergic interneurons. (cas.cz)
  • This disruption is thought to result from an autoantibody-mediated removal of a subset of the P/Q-type Ca2+ channels involved with neurotransmitter release. (medscape.com)
  • However, because presynaptic stores of ACh and the postsynaptic response to ACh remain intact, rapid repetitive stimulation or voluntary activation that aids in the release of quanta will raise the endplate potential above threshold and permit generation of muscle action potential. (medscape.com)
  • The excretion route is expected to be via the urine, because Guanidine Thiocyanate dissociates in body fluids into the corresponding ions, is highly water soluble and has a low molecular weight of 118 g/mol. (europa.eu)
  • Extracellularly, magnesium ions block neurosynaptic transmission by interfering with the release of acetylcholine. (medscape.com)
  • After oral exposure signs of systemic toxicity including death were observed in an acute toxicity study, thus absorption of Guanidine Thiocyanate has obviously occurred. (europa.eu)
  • calmodulin dependent enzyme, located in the endothelium, that releases NO in response to receptor or physical stimulation. (justia.com)
  • Guanidine apparently acts by enhancing the release of acetylcholine following a nerve impulse. (europa.eu)
  • The number of quanta released by a nerve impulse is diminished. (medscape.com)
  • Fatal bone-marrow suppression, apparently dose related, can occur with guanidine. (nih.gov)
  • Because guanidine is excreted in milk, patients on this drug should discontinue breastfeeding. (nih.gov)
  • Renal function may be affected in some patients receiving guanidine. (nih.gov)
  • Immediately following dilution out of 6M guanidine CRES3 rapidly transitioned into stable amyloid polygons, highly thioflavin T reactive structures with little or no oligomeric forms present, while CRES was distributed between both immature oligomeric and mature fibrillar amyloid forms (Fig 3A-C). CRES2 and cystatin E2 also immediately CD14 transitioned to amyloid after dilution and formed matrices, films and fibrils (Fig 3B). (smartrailexpo-europe.com)
  • [ 51 ] The ß-cells of K-channel-deficient islets have high basal Ca 2+ levels (at least twice the levels of controls) and show a greatly enhanced basal insulin release (i.e., the process of insulin release has been triggered by depolarization due to deleting the K-channels), but little or no augmentation of secretion is demonstrable when high glucose is the sole stimulus. (medscape.com)
  • Keep away from sources of ignition - No smoking.In case of contact with eyes, rinse immediately with plenty of water and seek medical advice.Wear suitable protective clothing, gloves and eye/face protection.In case of accident or if you feel unwell, seek medical advice immediately (show the label where possible).Avoid release to the environment. (alphachemikaindia.com)
  • Keep under argon.Wear suitable protective clothing and gloves.In case of accident or if you feel unwell, seek medical advice immediately (show the label where possible).Avoid release to the environment. (alphachemikaindia.com)
  • The NO released by each of the two constitutive enzymes acts as a transduction mechanism underlying several physiological responses. (justia.com)
  • An early pathophysiological feature of Alzheimer's disease that is associated with memory loss and cognitive deficits is a deficiency of acetylcholine as a result of selective loss of chol. (illumina.com)
  • The result is a prolonged effect of acetylcholine. (illumina.com)
  • No toxicokinetic studies are available for Guanidine Thiocyanate. (europa.eu)
  • Our own studies with isolated islets from SUR-1 knockout mice can be used to illustrate the distinction between fuel-induced triggering and neuro-endocrine augmentation or amplification of release (Fig. 3). (medscape.com)
  • The glucose-induced activation of intermediary metabolism (i.e., glycolysis, the pentose-P shunt, the citric acid cycle, alterations of amino acid and lipid catabolism, and synthesis) results in the generation of so-called "metabolic coupling factors" that mediate insulin release (Fig. 2 A and B ). The cytosolic levels of ATP and ADP are outstanding examples and represent probably the most important coupling factors. (medscape.com)
  • Levels of anilides, 2,6-dinitroanilines, chlorophenols, triclosan, and guanidines significantly increased in both farmworker and nonfarmworker households in 2011 vs. 2005. (nih.gov)