Bethanidine: A guanidinium antihypertensive agent that acts by blocking adrenergic transmission. The precise mode of action is not clear.Bretylium CompoundsMethylguanidine: A product of putrefaction. Poisonous.Guanethidine: An antihypertensive agent that acts by inhibiting selectively transmission in post-ganglionic adrenergic nerves. It is believed to act mainly by preventing the release of norepinephrine at nerve endings and causes depletion of norepinephrine in peripheral sympathetic nerve terminals as well as in tissues.Protriptyline: Tricyclic antidepressant similar in action and side effects to IMIPRAMINE. It may produce excitation.Guanidines: A family of iminourea derivatives. The parent compound has been isolated from mushrooms, corn germ, rice hulls, mussels, earthworms, and turnip juice. Derivatives may have antiviral and antifungal properties.Antihypertensive Agents: Drugs used in the treatment of acute or chronic vascular HYPERTENSION regardless of pharmacological mechanism. Among the antihypertensive agents are DIURETICS; (especially DIURETICS, THIAZIDE); ADRENERGIC BETA-ANTAGONISTS; ADRENERGIC ALPHA-ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; CALCIUM CHANNEL BLOCKERS; GANGLIONIC BLOCKERS; and VASODILATOR AGENTS.Chlorphentermine: A sympathomimetic agent that was formerly used as an anorectic. It has properties similar to those of DEXTROAMPHETAMINE. It has been implicated in lipid storage disorders and pulmonary hypertension. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1223)Phentermine: A central nervous system stimulant and sympathomimetic with actions and uses similar to those of DEXTROAMPHETAMINE. It has been used most frequently in the treatment of obesity.Encyclopedias as Topic: Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)Appetite Depressants: Agents that are used to suppress appetite.Aminorex: An amphetamine-like anorectic agent. It may cause pulmonary hypertension.Fenfluramine: A centrally active drug that apparently both blocks serotonin uptake and provokes transport-mediated serotonin release.Dexfenfluramine: The S-isomer of FENFLURAMINE. It is a serotonin agonist and is used as an anorectic. Unlike fenfluramine, it does not possess any catecholamine agonist activity.Phenmetrazine: A sympathomimetic drug used primarily as an appetite depressant. Its actions and mechanisms are similar to DEXTROAMPHETAMINE.Monoamine Oxidase Inhibitors: A chemically heterogeneous group of drugs that have in common the ability to block oxidative deamination of naturally occurring monoamines. (From Gilman, et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th ed, p414)Monoamine Oxidase: An enzyme that catalyzes the oxidative deamination of naturally occurring monoamines. It is a flavin-containing enzyme that is localized in mitochondrial membranes, whether in nerve terminals, the liver, or other organs. Monoamine oxidase is important in regulating the metabolic degradation of catecholamines and serotonin in neural or target tissues. Hepatic monoamine oxidase has a crucial defensive role in inactivating circulating monoamines or those, such as tyramine, that originate in the gut and are absorbed into the portal circulation. (From Goodman and Gilman's, The Pharmacological Basis of Therapeutics, 8th ed, p415) EC 1.4.3.4.Phenelzine: One of the MONOAMINE OXIDASE INHIBITORS used to treat DEPRESSION; PHOBIC DISORDERS; and PANIC.Tranylcypromine: A propylamine formed from the cyclization of the side chain of amphetamine. This monoamine oxidase inhibitor is effective in the treatment of major depression, dysthymic disorder, and atypical depression. It also is useful in panic and phobic disorders. (From AMA Drug Evaluations Annual, 1994, p311)Clorgyline: An antidepressive agent and monoamine oxidase inhibitor related to PARGYLINE.MedlinePlus: NATIONAL LIBRARY OF MEDICINE service for health professionals and consumers. It links extensive information from the National Institutes of Health and other reviewed sources of information on specific diseases and conditions.Commonwealth of Independent StatesConsumer Health Information: Information intended for potential users of medical and healthcare services. There is an emphasis on self-care and preventive approaches as well as information for community-wide dissemination and use.Australia: The smallest continent and an independent country, comprising six states and two territories. Its capital is Canberra.Social Media: Platforms that provide the ability and tools to create and publish information accessed via the INTERNET. Generally these platforms have three characteristics with content user generated, high degree of interaction between creator and viewer, and easily integrated with other sites.Micronesia: The collective name for islands of the Pacific Ocean east of the Philippines, including the Mariana, PALAU, Caroline, Marshall, and Kiribati Islands. (From Webster's New Geographical Dictionary, 1988, p761 & Room, Brewer's Dictionary of Names, 1992, p350)Mydriasis: Dilation of pupils to greater than 6 mm combined with failure of the pupils to constrict when stimulated with light. This condition may occur due to injury of the pupillary fibers in the oculomotor nerve, in acute angle-closure glaucoma, and in ADIE SYNDROME.3,4-Methylenedioxyamphetamine: An amphetamine derivative that inhibits uptake of catecholamine neurotransmitters. It is a hallucinogen. It is less toxic than its methylated derivative but in sufficient doses may still destroy serotonergic neurons and has been used for that purpose experimentally.N-Methyl-3,4-methylenedioxyamphetamine: An N-substituted amphetamine analog. It is a widely abused drug classified as a hallucinogen and causes marked, long-lasting changes in brain serotonergic systems. It is commonly referred to as MDMA or ecstasy.Psychotropic Drugs: A loosely defined grouping of drugs that have effects on psychological function. Here the psychotropic agents include the antidepressive agents, hallucinogens, and tranquilizing agents (including the antipsychotics and anti-anxiety agents).Alexander Disease: Rare leukoencephalopathy with infantile-onset accumulation of Rosenthal fibers in the subpial, periventricular, and subependymal zones of the brain. Rosenthal fibers are GLIAL FIBRILLARY ACIDIC PROTEIN aggregates found in ASTROCYTES. Juvenile- and adult-onset types show progressive atrophy of the lower brainstem instead. De novo mutations in the GFAP gene are associated with the disease with propensity for paternal inheritance.Amphetamines: Analogs or derivatives of AMPHETAMINE. Many are sympathomimetics and central nervous system stimulators causing excitation, vasopressin, bronchodilation, and to varying degrees, anorexia, analepsis, nasal decongestion, and some smooth muscle relaxation.Gemfibrozil: A lipid-regulating agent that lowers elevated serum lipids primarily by decreasing serum triglycerides with a variable reduction in total cholesterol.Cyclohexanecarboxylic AcidsAmines: A group of compounds derived from ammonia by substituting organic radicals for the hydrogens. (From Grant & Hackh's Chemical Dictionary, 5th ed)Anticonvulsants: Drugs used to prevent SEIZURES or reduce their severity.Central Nervous System Stimulants: A loosely defined group of drugs that tend to increase behavioral alertness, agitation, or excitation. They work by a variety of mechanisms, but usually not by direct excitation of neurons. The many drugs that have such actions as side effects to their main therapeutic use are not included here.Nordefrin: A norepinephrine derivative used as a vasoconstrictor agent.Deoxyepinephrine: Sympathomimetic, vasoconstrictor agent.Methyldopa: An alpha-2 adrenergic agonist that has both central and peripheral nervous system effects. Its primary clinical use is as an antihypertensive agent.Coptis: A plant genus of the family RANUNCULACEAE. Members contain BERBERINE and other isoquinoline ALKALOIDS.Tryptamines: Decarboxylated monoamine derivatives of TRYPTOPHAN.Bufotenin: A hallucinogenic serotonin analog found in frog or toad skins, mushrooms, higher plants, and mammals, especially in the brains, plasma, and urine of schizophrenics. Bufotenin has been used as a tool in CNS studies and misused as a psychedelic.Designer Drugs: Drugs designed and synthesized, often for illegal street use, by modification of existing drug structures (e.g., amphetamines). Of special interest are MPTP (a reverse ester of meperidine), MDA (3,4-methylenedioxyamphetamine), and MDMA (3,4-methylenedioxymethamphetamine). Many drugs act on the aminergic system, the physiologically active biogenic amines.Psilocybine: The major of two hallucinogenic components of Teonanacatl, the sacred mushroom of Mexico, the other component being psilocin. (From Merck Index, 11th ed)Copyright: It is a form of protection provided by law. In the United States this protection is granted to authors of original works of authorship, including literary, dramatic, musical, artistic, and certain other intellectual works. This protection is available to both published and unpublished works. (from Circular of the United States Copyright Office, 6/30/2008)Organizations, Nonprofit: Organizations which are not operated for a profit and may be supported by endowments or private contributions.Patents as Topic: Exclusive legal rights or privileges applied to inventions, plants, etc.Computer Security: Protective measures against unauthorized access to or interference with computer operating systems, telecommunications, or data structures, especially the modification, deletion, destruction, or release of data in computers. It includes methods of forestalling interference by computer viruses or so-called computer hackers aiming to compromise stored data.Confidentiality: The privacy of information and its protection against unauthorized disclosure.Sympathomimetics: Drugs that mimic the effects of stimulating postganglionic adrenergic sympathetic nerves. Included here are drugs that directly stimulate adrenergic receptors and drugs that act indirectly by provoking the release of adrenergic transmitters.Cacodylic Acid: An arsenical that has been used as a dermatologic agent and as an herbicide.Dietary Supplements: Products in capsule, tablet or liquid form that provide dietary ingredients, and that are intended to be taken by mouth to increase the intake of nutrients. Dietary supplements can include macronutrients, such as proteins, carbohydrates, and fats; and/or MICRONUTRIENTS, such as VITAMINS; MINERALS; and PHYTOCHEMICALS.Research Design: A plan for collecting and utilizing data so that desired information can be obtained with sufficient precision or so that an hypothesis can be tested properly.Child, Hospitalized: Child hospitalized for short term care.

Drinking behaviour in the cat induced by renin, angiotensin I, II and isoprenaline. (1/17)

1. Angiotensin I, II and hog renin, infused into the lateral cerebral ventricles (I.C.V.) of water replete cats, each induced water drinking behaviour. 2. Intravenous infusion of high doses of angiotensin I or II also elicited a drinking response. The dipsogenic effect of I.V. renin was not marked. 3. Drinking in response to I.C.V. angiotensin II was abolished after autonomic ganglion blockade with I.V. hexamethonium or pempidine and was significantly reduced after I.V. atropine methonitrate. 4. The dipsogenic response to I.C.V. angiotensin II was unaffected by either peripheral adrenergic neurone blockade with I.V. bethanidine, alpha-adrenoceptor blockade with phentolamine or beta-adrenoceptor blockade with sotalol. 5. Atropine, atropine methonitrate, hexamethonium and pempidine given I.C.V did not inhibit the diposgenic response to I.C.V. angiotensin II. 6. Bethanidine I.C.V. produced a dose related reduction in the dipsogenic response to I.C.V. angiotensin II. 7. The alpha-adrenoceptor blocking agents tolazoline and phenoxybenzamine given I.C.V did not affect angiotensin induced drinking but the response was regularly inhibited by phentolamine I.C.V. 8. The beta-adrenoceptor blocking agents propranolol and practolol given I.C.V. each inhibited angiotensin induced drinking. The L-isomer of propranolol was a more effective blocker than the D-isomer. 9. Isoprenaline given I.C.V induced drinking in ten of sixteen cats. Subcutaneous administration of isoprenaline also elicited drinking but the onset of the response was delayed and the amount consumed slightly less than after I.C.V infusion.  (+info)

Effects of methyldopa on prolactin and growth hormone. (2/17)

The effects of administration of methyldopa on serum prolactin and growth hormone (GH) concentrations in hypertensive patients were studied. Single doses of methyldopa (750 or 1000 mg) significantly increased serum prolactin levels, peak concentrations occurring four to six hours after drug administrations. Long-term methyldopa treatment was associated with threefold to fourfold increases in basal prolactin levels compared with those in normal subjects. In patients treated with methyldopa for two to three weeks the GH response to insulin hypoglycaemia was significantly greater than in normal subjects and untreated hypertensive patients. In contrast, patients treated for prolonged periods (mean 13-4 months) had a GH reponse indistinguishable from normal.  (+info)

Factors predisposing to postural hypotensive symptoms in the treatment of high blood pressure. (3/17)

Symptoms due to orthostatic and exertional hypotension occurred in 23-4 per cent of 448 hypertensive patients treated with guanethidine, debrisoquine, or bethanidine. Symptoms were significantly more frequent in patients treated with guanethidine than in those treated with bethanidine or debrisoquine. Women rather than men and patients with radiological evidence of cardiomegaly, electrocardiographic evidence of left ventricular hypertrophy, or ST/T wave changes, developed these symptoms significantly more often than other patients. A raised blood urea was found more frequently in patients with postural hypotensive symptoms. Characteristically guanethidine produced early morning postural hypotensive symptoms, wheras hypotensive symptoms caused by bethanidine and debrisoquine occurred at other times of the day and particularly one to two hours after tablet ingestion. Debrisoquine and guanethidine had a significantly greater negative chronotropic effect than bethanidine. It is suggested that negative chronotropic effects of these drugs may potentiate hypotensive symptoms in patients with cardiovascular, renal, or cerebrovascular disease. It should be possible to minimize symptoms of postural hypotension by attention to predisposing factors and selection of treatment accordingly.  (+info)

The response of the circular muscle layer of the guinea-pig isolated vas deferens to transmural electrical stimulation. (4/17)

1 Four preparations are described for the isolation of the response of the circular muscle of the guinea-pig vas deferens. These are the ;Furchgott' strip, the ;Vane' strip, the chain preparation and the perfused preparation.2 The four preparations were stimulated transmurally with pulses of supramaximal voltage. The threshold pulse width to which the strips and the perfused preparation responded was 0.025 ms and the maximum responses occurred at 0.1 ms. The threshold frequency was 2 Hz for strip and perfused preparations, the maxima being 20 or 50 Hz for strip preparations and 100 Hz for perfused preparations. The effect of varying the number of pulses per train was also investigated on the perfused vas. Responses occurred to train lengths of 8, 16, 32, 128 pulses, the maximum response being given at 128 pulses at 100 Hz; 256 pulses per train did not produce a further increase in response. The perfused preparation exhibited an after-response at certain frequencies and train lengths.3 Tetrodotoxin and the local anaesthetics, procaine and lignocaine, reversibly abolished the responses of strip and perfused preparations to transmural stimulation.4 The response to intramural nerve fibre stimulation was abolished by guanethidine or bethanidine; this abolition was reversed by dexamphetamine. Noradrenaline contracted strip preparations of circular muscle and raised the pressure in perfused preparations; noradrenaline was competitively antagonized by thymoxamine. The major part of the motor innervation of the circular layer seems to be noradrenergic.  (+info)

Potassium channel blockade: A mechanism for suppressing ventricular fibrillation. (5/17)

The suppression of ventricular fibrillation by antidysrhythmic drugs is well correlated with their ability to block potassium channels in nerve and cardiac membranes. Blockade of potassium channels reduces electrical inhomogeneities in action potential and conduction parameters that lead to ventricular fibrillation. These actions tend to effectively decrease the electrical size of the heart, which suggests a mechanism for antifibrillatory drug action. The receptor sites for antifibrillatory drug action (IK blockade) appear to be on the outside of the cardiac membrane whereas receptors for antiarrhythmic drug action (INa blockade) appear to be on the inside of the cardiac membrane.  (+info)

Effect of mianserin hydrochloride on peripheral uptake mechanisms for noradrenaline and 5-hydroxytryptamine in man. (6/17)

1. Mianserin seems to have little effect on peripheral noradrenaline (NA) re-uptake mechanisms as shown by its lack of effects on the tyramine dose and NA dose/pressor response. 2. Mianserin has no effect on the hypotensive action of bethanidine. 3. Mianserin in vivo has a significant action on platlet transport (Vmax) of 5-hydroxytryptamine (5-HT), which changes toward normal values in depressive patients on the drug. This action is not observed in vitro. 4. It is possible that a metabolite of mianserin is responsible for this effect, and that this may be of therapeutic importance.  (+info)

Cardiovascular responses to mianserin hydrochloride: a comparison with tricyclic antidepressant drugs. (7/17)

1. The cardiovascular responses of mianserin hydrochloride and tricyclic antidepressant drugs were investigated using non-invasive methods of cardiac investigation. A study of the interaction of mianserin and antihypertensive drug therapy is reported. 2. In six normal volunteers, mianserin hydrochloride 20 mg was shown to prolong the corrected Q-T interval at 150 min (P less than 0.001). It did not affect heart rate, systolic time intervals or the peak normalized derivative of the apexcardiogram. Amitriptyline 50 mg increased the corrected pre-ejection period interval (PEPI) and the PEP/left ventricular ejection time (LVET) ratio of the systolic time intervals at 150 min (P less than 0.001). Q-T interval was shortened at 90 minutes. 3. In a double-blind patient study, clomipramine increased heart rate, P-R interval, QRS and corrected Q-T interval in one patient at 2 weeks. Mianserin prolonged corrected Q-T interval at 1 week but this returned to the pretreatment time by 2 weeks in two patients. 4. In an open study, mianserin 20 mg three times daily did not antagonize the hypotensive action of propranolol or propranolol and hydrallazine in three patients. 5. In a double-blind study in three patients with desmethylimipramine 25 mg three times daily, mianserin 20 mg three times daily did not antagonize the hypotensive action of either guanethidine or bethanidine.  (+info)

New drugs in hypertension. (8/17)

Clonidine, propranolol, bethanidine and debrisoquine effectively decrease blood pressure by suppressing renin secretion or interfering with function of the sympathetic nervous system. In man these compounds exert an antihypertensive effect within several hours or days and their duration of action is sufficient to permit administration twice or thrice daily. Clonidine and propranolol are especially useful if sexual dysfunction or postural hypotension is undesirable. Although bethanidine and debrisoquine may produce these adverse effects, they are beneficial in severe hypertension and produce fewer side effects than guanethidine. Clonidine frequently causes sedation, and rebound hypertension may occur with sudden cessation of therapy. Injudicious use of propranolol may provoke heart failure or asthma in susceptible individuals. The combination of a thiazide diuretic with propranolol and one of hydralazine, bethanidine and debrisoquine may be used to treat severe or complicated hypertension.  (+info)

Exertional hypotension in thoracic spinal cord injury: case report.: Exertional hypotension is well described in quadraplegics, but there are few descriptions o
glutamate oxaloacelate transarninase [GOT] , glutamate. pyruvate transminase [GPT] - in to the culture medium. Cytotoxicity was also assessed by applying cell viability test, where dead cells aquired staining while living cells remained unstained. This study showed that methyldopa produced a damaging effect on cultured rat hepatocytecs and increasing the number of dead cells. The inclusion of albumin in the culture system provided a good protection to s against the damaging effect of methyldopa. Its probably advisable to provide a maximum availability of albumin ...
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ERS -Early repolarisation syndrome is known as a benign ECG finding for many decades .Now it is beginning to look dangerous as evidence is accumulating it may have a link with ventricular arrhythmias. ERS represents complex changes in ionic movements during cardiac repolarisation . (To be specific , it is due to a functional…
Methyldopa is an alpha 2 agonist. Methyldopa is useful in treating hypertension mostly in pregnant woman. The duration of action of methyldopa is 24 hours.
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The stress of foot shock in rats induces large decreases in the level of brain norepinephrine but does not greatly alter the concentration of serotonin or dopamine in brain. These decrements in norepinephrine are not limited to any region and occur uniformly throughout the brain. However, absolute levels of these amines are not a true indicator of their dynamic state. By various techniques it could be demonstrated that the stress of foot shock accelerates the metabolism of dopamine and serotonin to the same degree as norepinephrine; the only difference being that dopamine and serotonin are rapidly resynthesized, whereas norepinephrine in the brain cannot be regenerated at the same rate. Furthermore, the increased catabolism of brain norepinephrine with stress is blocked by monoamine oxidase inhibitors, whereas catechol-O-methyltransferase inhibitors do not impede accelerated degradation.. ...
d-Amphetamine is markedly more potent an inhibitor of catecholamine uptake by norepinephrine neurons in the brain than is 1-amphetamine, whereas the two isomers are equally active in inhibiting catecholamine uptake by the dopamine neurons of the corpus striatum. In behavioral studies, d-amphetamine is ten times as potent as 1-amphetamine in enhancing locomotor activity, while it is only twice as potent in eliciting a compulsive gnawing syndrome. This suggests that the locomotor stimulation induced by amphetamine involves central norepinephrine, while dopamine neurons play an important role in the induced compulsive gnawing behavior. Assessment of differential actions of d- and 1-amphetamine may be an efficient method to differentiate behaviors involving norepinephrine or dopamine in the brain. ...
After bilateral olfactory bulbectomy in rats a significant increase of norepinephrine (NE) level in the hypothalamus was found. However, no difference was observed between hypothalamic NE turnover of bulbectomized and sham operated animals. In the amygdaloid cortex the NE level was not affected by bulbectomy. In this area, however, the ... read more NE turnover appeared to be decreased after bulbectomy. The latter finding may be related to the deficits in passive avoidance behaviour as found in bulbectomized rats. show less ...
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Signs of Methyldopa - Teratogenic Agent including medical signs and symptoms of Methyldopa - Teratogenic Agent, symptoms, misdiagnosis, tests, common medical issues, duration, and the correct diagnosis for Methyldopa - Teratogenic Agent signs or Methyldopa - Teratogenic Agent symptoms.
The neuropharmacology course will discuss the drug-induced changes in functioning of the nervous system. The specific focus of this course will be to provide a description of the cellular and molecular actions of drugs on synaptic transmission. This course will also refer to specific diseases of the nervous system and their treatment in addition to giving an overview of the techniques used for the study of neuropharmacology. This course is offered during the Independent Activities Period (IAP) ...
repolarisation definition - the restoration of the usual electrical polarity of a nerve or muscle cell membrane after reversal of its polarity while a nerve impulse or muscle contraction ...
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Background: Assessing propensity to torsades de pointes (TdP) when exposed to QT-prolonging drug is challenging because baseline QT-prolongation has limited predictive value for identifying risk of TdP. The aim of this study was to determine whether computer-based repolarization morphology parameters could identify individuals who developed drug-induced TdP.. Method: Five-minute standard digital 12-lead ECGs were acquired at baseline and after a controlled sotalol challenge (2 mg/kg BW, i.v.) in 34 cardiac patients of whom 17 had a history of TdP (+TdPs) in the context of a QT prolonging drug and 17 had no history of TdP (-TdPs).Computerized ECG parameters including QT, TpTe (T peak to T end interval) and a morphological measure of the duration of the early part of the repolarization interval (ERD) were implemented. All parameters were corrected for the effect of heart rate (HR).. Results: There were 9 females among the + TdP patients and 12 females in the -TdP group (p = 0.8). The drugs ...
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I then used a microbore pipe bender to make the bends in the pipe. Its a handy little tool, but unfortunately they put far too much paint on it, meaning the measuring bits and the 6mm tube channel was too small, meaning the tube wouldnt get equal pressure around it when bending and would deform too much for my liking. After a quick bit of paintstripping with Nitromors I bent the tubes for insertion into the copper wall. This was a bit fiddly; in order for the bends to line up exactly with the drilled holes I needed to know amount of length the bend took. After a few annoying mishaps, annealing and restraightening I got the tubes bent accurately ...
Type 1 Diabetes is an autoimmune condition in which segments of the immune system cause the destruction of insulin producing cells in the pancreas, leaving individuals with an impaired ability to control blood glucose levels. Currently there is no cure for Type 1 Diabetes and the treatments involve lifelong insulin administration and careful monitoring of blood glucose levels. Long-term complications like cardiovascular disease, nerve damage, and retina damage, may result. Previous studies have shown that improvement in the control of blood glucose can reduce the risks from these long-term complications. Residual insulin production, typically within the first few years following diagnosis, helps to reduce an individuals need to supplement insulin by injection or pump. This effect helps in maintaining the bodys ability to regulate blood glucose levels and reducing the needs of external insulin.. Methyldopa, or Aldomet, has been approved by the Food and Drug Administration and is commonly used ...
SUPELCOSIL LC-F HPLC columns contain a pentafluorophenyl functional group that offers unique selectivity, different from traditional reversed-phase columns, for halogenated compounds, esters, ketones, bases, and taxanes (including taxol). Suitable for L43 per USP.
Abnormally rapid repolarisation of the infarcted muscle (accelerated opening of K+ channels). Current flow out of infarct (normal region negative relative to infarct). Occurs within seconds of infarction and last a few minutes ...
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Hi my psychiatrist has offered me mianserin but I can t find any reviews online it s like it doesn t exist, please has anyone here tried it? May of been called Tolvon in other countries....it s making my anxiety high that I can t find anything to do with this antidepressant, I know it s an old antidepressant I just want some reviews....thanks for reading
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Mice were rendered dependent on morphine by the subcutaneous pellet implantation technique. After three days, the pellet was removed and six hours later, withdrawal jumping was precipitated by subcutaneous naloxone. Brain dopamine (DA), norepinephrine and serotonin were measured at various intervals after naloxone. A sudden increase in DA was noted to occur in dependent mice that jumped but not in those that failed to jump. The increase in DA after naloxone occurred within 2 minutes and was maximum between 5 to 10 minutes when the incidence of the precipitated morphine withdrawal jumping response was at a peak. Brain norepinephrine and serotonin levels remained unaltered after the naloxone challenge in both morphine-dependent and naive groups of animals. The increase in brain DA was greatest in the cortical-striatal area of mice. Similar regional brain studies in the morphine-dependent rat indicated that the greatest elevation in DA occurred in the corpus striatum. Administration of ...
If you have a fever and there seems to be no reason for it, check with your doctor. This is especially important during the first few weeks you take methyldopa, since fever may be a sign of a serious reaction to this medicine.. Before having any kind of surgery (including dental surgery) or emergency treatment, make sure the medical doctor or dentist in charge knows that you are taking this medicine.. Methyldopa may cause some people to become drowsy or less alert than they are normally. This is more likely to happen when you begin to take it or when you increase the amount of medicine you are taking. Make sure you know how you react to this medicine before you drive, use machines, or do anything else that could be dangerous if you are not alert.. Dizziness, lightheadedness, or fainting may occur, especially when you get up from a lying or sitting position. Getting up slowly may help, but if the problem continues or gets worse, check with your doctor.. Methyldopa may cause dryness of the mouth. ...
In this paper, Freis evaluated the newly developed ganglion-blocking agent, methyldopa. He reported that it exhibited fewer side effects than a similar drug, guanethidine, yet it was not favored by patients since it required them to take a larger number of tablets at a greater frequency ...
TY - JOUR. T1 - Opiate antagonist facilitation of time-dependent memory processes. T2 - Dependence upon intact norepinephrine function. AU - Gallagher, Michela. AU - Rapp, Peter R.. AU - Fanelli, Richard J.. PY - 1985/11/18. Y1 - 1985/11/18. N2 - Post-training administration of opiate antagonists improves retention of recent learning in laboratory animals tested on a variety of tasks. We examined the possibility that this effect of opiate antagonist treatment might be due to release of brain norepinephrine (NE) function from opioid peptide inhibition. The behavioral testing procedure in these experiments consisted of one-trial passive avoidance conditioning. Rats received post-training treatments immediately after the training trial and retention was tested 24 h later. Lesions of the dorsal noradrenergic bundle (DNB) that were induced by 6-hydroxydopamine (6-OHDA) were found to prevent the memory enhancing effect of post-training naloxone administration. The memory enhancing effect of naloxone ...
It is important to recognize that a positive Coombs test, hemolytic anemia, and liver disorders may occur with methyldopa therapy.The rare occurrences of hemolytic anemia or liver disorders could lead to potentially fatal complications unless properly recognized and managed. Read this section carefully to understand these reactions. With prolonged methyldopa therapy, 10% to 20% of patients develop a positive direct Coombs test which usually occurs between 6 and 12 months of methyldopa therapy. Lowest incidence is at daily dosage of 1 g or less. This on rare occasions may be associated with hemolytic anemia, which could lead to potentially fatal complications. One cannot predict which patients with a positive direct Coombs test may develop hemolytic anemia.. Prior existence or development of a positive direct Coombs test is not in itself a contraindication to use of methyldopa. If a positive Coombs test develops during methyldopa therapy, the physician should determine whether hemolytic anemia ...
... (Voranil) was developed by Ciba in the 1960s[1] and is an anorectic drug of the amphetamine class.[2] It is the 2-chloro analogue of the better known appetite suppressant phentermine, and is the 2-chloro positional isomer of chlorphentermine. Clortermine produces very low rates of self-administration in animals similarly to chlorphentermine,[3] and as a result it likely does not act on dopamine. Instead, it may act as a serotonin and/or norepinephrine releasing agent.[citation needed] ...
... is a drug and research chemical used in scientific studies. It acts as a monoamine releasing agent with 20- to 48-fold selectivity for releasing dopamine versus serotonin. It is most efficacious as a releaser of norepinephrine, with an ec50 of 109/41.4/5246nM for DA/NE/5HT, respectively .[1] It has a fast onset of action and a short duration.[1] It also functions as a monoamine oxidase inhibitor (MAOI) with preference for MAO-A.[2] ...
DMA is considered a Schedule 9 prohibited substance in Australia under the Poisons Standard (October 2015).[6] A Schedule 9 substance is a substance which may be abused or misused, the manufacture, possession, sale or use of which should be prohibited by law except when required for medical or scientific research, or for analytical, teaching or training purposes with approval of Commonwealth and/or State or Territory Health Authorities.[6] ...
... ("3,4-MDPEA" or just "MDPEA"), also known as homopiperonylamine, is a substituted phenethylamine formed by adding a methylenedioxy group to phenethylamine. It is structurally similar to MDA, but without the methyl group at the alpha position. According to Alexander Shulgin in his book PiHKAL, MDPEA appears to be biologically inactive. This is likely because of extensive first-pass metabolism by the enzyme monoamine oxidase. However, if MDPEA were either used in high enough of doses (e.g., 1-2 grams), or in combination with a monoamine oxidase inhibitor (MAOI), it is probable that it would become sufficiently active, though it would likely have a relatively short duration of action. This idea is similar in concept to the use of selective MAOA inhibitors and selective MAOB inhibitors in augmentation of dimethyltryptamine (DMT) and phenethylamine (PEA), respectively. ...
Alexander Shulgin conducted research on methylenedioxy compounds in the 1960s. In a 1967 lab notebook entry, Shulgin briefly mentioned a colleague's report of no effect from the substance with a 100 mg dose.[4] Shulgin later characterized the substance in his book PiHKAL.[3] In the United States, MDEA was introduced recreationally in 1985 as a legal substitute to the newly banned MDMA.[2] MDEA was made a Schedule 1 substance in the United States on August 13, 1987 under the Federal Analog Act.[1] ...
... (Gevilon) is a stimulant drug. It has been used for the treatment of alcoholism[1] and for increasing motivation in elderly patients,[2] but is now mainly used for the treatment of hyperlipoproteinaemia. [3][4] It is chemically similar to the anticonvulsant gabapentin, with a hydroxyl group replacing the amine. The latter use may be incorrectly assigned, as "Gevilon" has been used as a trade name for gemfibrozil, a well-known drug for dislypidemia. ...
Difluoromethylenedioxyamphetamine (DiFMDA) is a substituted derivative of 3,4-methylenedioxyamphetamine (MDA), which was developed by Daniel Trachsel and coworkers, along with the corresponding fluorinated derivatives of MDMA, MDEA, BDB and MBDB, with the aim of finding a non-neurotoxic drug able to be used as a less harmful substitute for entactogenic drugs such as MDMA. Since a major route of the normal metabolism of these compounds is scission of the methylenedioxy ring, producing neurotoxic metabolites such as alpha-methyldopamine, it was hoped that the difluoromethylenedioxy bioisostere would show increased metabolic stability and less toxicity.[1][2] These compounds have not yet been tested in animals to verify whether they show similar pharmacological activity to the non-fluorinated parent compounds, although in vitro binding studies show DFMDA to have a SERT affinity in between that of MDA and MDMA.[3] However, there is known to be a lack of bulk tolerance at this position of the ...
Amphetamines like MDMA, MDEA, MDA, and MBDB, among other relatives (see MDxx), are recreational drugs termed entactogens. They act as serotonin-norepinephrine-dopamine releasing agents (SNDRAs) and also agonize serotonin receptors such as those in the 5-HT2 subfamily. Fenfluramine, chlorphentermine, and aminorex, which are also amphetamines and relatives, were formerly used as appetite suppressants but were discontinued due to concerns of cardiac valvulopathy. This side effect has been attributed to their additional action of potent agonism of the 5-HT2B receptor. The designer drug 4-methylaminorex, which is an SNDRA and 5-HT2B agonist, has been reported to cause this effect as well. Many tryptamines, such as DMT, DET, DPT, DiPT, psilocin, and bufotenin, are SRAs as well as non-selective serotonin receptor agonists.[3] These drugs are serotonergic psychedelics, which is a consequence of their ability to activate the 5-HT2A receptor. αET and αMT, also tryptamines, are SNDRAs and non-selective ...
Text is available under the Creative Commons Attribution-ShareAlike License; additional terms may apply. By using this site, you agree to the Terms of Use and Privacy Policy. Wikipedia® is a registered trademark of the Wikimedia Foundation, Inc., a non-profit organization ...
The LD50 for methylhexanamine is 39 mg/kg in mice and 72.5 mg/kg in rats, when administered intravenously.[7]:95[16]:110 The FDA has stated that methylhexanamine "is known to narrow the blood vessels and arteries, which can elevate blood pressure and may lead to cardiovascular events ranging from shortness of breath and tightening in the chest to heart attack".[17] Numerous adverse events and at least five deaths have been reported in association with methylhexanamine-containing dietary supplements.[3] A 2012 review by a panel convened by the U.S. Department of Defense to study whether the military should ban methylhexanamine supplements from stores on its bases concluded that: "The existing evidence does not conclusively establish that DMAA-containing substances are causally-associated with adverse medical events. However, a consistent theme among the studies is that DMAA use potentially affects cardiovascular function, just as other sympathomimetic stimulants. Without further rigorous study ...
Drug discrimination studies showed that 5-methyl-MDA substitutes for MDA, MMAI, and LSD, but not amphetamine, suggesting that it produces a mix of entactogen and hallucinogenic effects without any stimulant effects.[2]. 5-Methyl-MDA acts as a selective serotonin releasing agent (SSRA) with IC50 values of 107nM, 11,600nM, and 1,494nM for serotonin, dopamine, and norepinephrine efflux.[1] It is over 5x more potent than MDA, with a suitable active dose possibly being around 15-25 mg.[1][2] Subsequent testing, however, has found that it is not as potent as once thought and is active at at least 100mg. 2-Methyl-MDA is also much more potent than MDA, but is not quite as potent as 5-methyl-MDA.[1] 6-methyl-MDMA (also known as Madam-6) is mostly inactive, likely due to steric hindrance.[1][3]. Recent research has used data on 2-methyl-MDA and 5-methyl-MDA to help guide computer modeling of the serotonin transporter complex.[4]. ...
The family of drugs typified by MDMA produce their effects through multiple mechanisms of action in the body, and consequently produce three distinct cues which animals can be trained to respond to: a stimulant cue typified by drugs such as methamphetamine, a psychedelic cue typified by drugs such as LSD and DOM, and an "entactogen-like" cue which is produced by drugs such as MDAI and MBDB. These drugs cause drug-appropriate responses in animals trained to recognize the effects of MDMA, but do not produce responses in animals trained selectively to respond to stimulants or hallucinogens. Because these compounds selectively release serotonin in the brain but have little effect on dopamine or noradrenaline levels, they can produce empathogenic effects but without any stimulant action, instead being somewhat sedating.[4][5][6][7][8][9][10] Very high doses can be fatal in rats with a 50% fatality rate for those subcutaneously injected with 28 mg/kg of MDAI. This is a result of the way serotonin ...
... (INN), also known as 2-methylamphetamine, is a stimulant drug of the amphetamine class. In animal drug discrimination tests it substituted for dextroamphetamine more closely than either 3- or 4-methylamphetamine, although with only around 1/10 the potency of dextroamphetamine itself.[1] ...
... (trade names Apsedon, Desopimon, Lucofen) is a serotonergic appetite suppressant of the amphetamine family. Developed in 1962, it is the 4-chloro derivative of the better known appetite suppressant phentermine,[1] which is still in current use. Chlorphentermine acts as a highly selective serotonin releasing agent (SRA).[2] It is not a psychostimulant and has little or no abuse potential, but is classed as a Schedule III drug in the USA due mainly to its similarity to other appetite suppressants such as diethylpropion which have been more widely abused. It is no longer used due mainly to safety concerns, as it has a serotonergic effects profile similar to other withdrawn appetite suppressants such as fenfluramine and aminorex which were found to cause pulmonary hypertension and cardiac fibrosis following prolonged use.[3] The plasma half-life is about five days.[4] It was withdrawn from the market in the UK in 1974.[4] ...
... (Gewodin, Gewolen) is a nonsteroidal anti-inflammatory agent (NSAID) of the pyrazolone series which is available over-the-counter in some countries such as Taiwan.[1][2][3] It has analgesic, anti-inflammatory, and antipyretic effects.[1][2] Famprofazone has been known to produce methamphetamine as an active metabolite, with 15-20% of an oral dose being converted to it.[4][5] As a result, famprofazone has occasionally been implicated in causing positives on drug tests for amphetamines.[3] ...
Giugliano D, Luyckx A, Binder D, Lefebvre P. Comparative effects of metformin and indanorex in the treatment of reactive hypoglycemia. International Journal of Clinical Pharmacology and Biopharmacy. 1979 Feb;17(2):76-81. ...
... is a class of prescription drugs in India appearing as an appendix to the Drugs and Cosmetics Rules, 1945 introduced in 1945. These are drugs which cannot be purchased over the counter without the prescription of a qualified doctor.The manufacture and sale of all drugs are covered under the Drugs and Cosmetics Act and Rules. It is revised at times based on the advice of the Drugs Technical Advisory Board, part of the Central Drugs Standard Control Organization[1] in the Ministry of Health and Family Welfare. The most recent schedule H (2006) lists 536 drugs from abacavir to zuclopenthixol.[2] However, enforcement of Schedule H laws in India is lax, compared to the more restrictive Schedule X, for which a mandatory documentation trail must be maintained.[3] ...
ഗുരുതരമായ ഭവിഷ്യത്തുകൾക്ക് കാരണമാകുന്ന ലഹരിമരുന്നാണ് മെത്തലീൻഡയോക്സി മെത്താംഫീറ്റമിൻ. സിന്തറ്റിക് ഡ്രഗ്‌സ് വിഭാഗത്തിൽപ്പെടുന്ന ലഹരിവസ്തു മോളി, എക്‌സ്, എക്സ്റ്റസി,എം.ഡി.എം.എ എന്ന വിളിപ്പേരുകളിലും അറിയപ്പെടുന്നു.ചികിത്സാരംഗത്ത് ഇത് ഉപയോഗിക്കുന്നതിനു സ്വീകാര്യത ലഭിച്ചിട്ടില്ല[9].നിശാപാർട്ടികളിൽ പങ്കെടുക്കുന്നവരാണ് ഇവ കൂടുതലായി ഉപയോഗിക്കുന്നത്. കൂടുതൽനേരം ലഹരി ...
Bethanidine Bretylium Guanadrel Guanazodine Guanclofine Guanethidine Guanoxan Oxidopamine (6-hydroxydopamine). ...
... bethanidine MeSH D02.078.370.141 --- biguanides MeSH D02.078.370.141.075 --- buformin MeSH D02.078.370.141.100 --- ...
Betanidine (or bethanidine) is a sympatholytic drug. Dibenamine (N,N-Dibenzyl-2-chloroethanamine) DE 824208 (1951). ... Phenoxybenzamine B. N. C. Prichard; A. W. Johnston; I. D. Hill & M. L. Rosenheim (1968). "Bethanidine, Guanethidine, and ...
... causes arterial/arteriolar vasodilation leading to a decrease in blood pressure by activating peripheral D1 receptors.[5] It decreases afterload and also promotes sodium excretion via specific dopamine receptors along the nephron. The renal effect of fenoldopam and dopamine may involve physiological antagonism of the renin-angiotensin system in the kidney.[6] In contrast to dopamine, fenoldopam is a selective D1 receptor agonist with no effect on beta adrenoceptors, although there is evidence that it may have some alpha-1 [7] and alpha-2 adrenoceptor antagonist activity.[5] D1 receptor stimulation activates adenylyl cyclase and raises intracellular cyclic AMP, resulting in vasodilation of most arterial beds, including renal, mesenteric, and coronary arteries.[8] to cause a reduction in systemic vascular resistance. Fenoldopam has a rapid onset of action (4 minutes) and short duration of action (, 10 minutes) and a linear dose-response relationship at usual clinical doses.[9] ...
InChI=1S/C32H38N2O8/c1-37-24-12-17(13-25(38-2)29(24)39-3)31(35)42-26-14-18-16-34-11-10-20-19-8-6-7-9-22(19)33-28(20)23(34)15-21(18)27(30(26)40-4)32(36)41-5/h6-9,12-13,18,21,23,26-27,30,33H,10-11,14-16H2,1-5H3/t18-,21+,23-,26-,27+,30+/m1/s1 ...
Trimetaphan is a sulfonium compound and therefore carries a positive charge. Being charged, it cannot cross lipid cell membranes, such as those that comprise the blood-brain barrier. Due to this, trimethaphan does not have any effect on the central nervous system. The ciliary muscle of the eye functions to round the lens for accommodation and is controlled mainly by parasympathetic system input. With administration of a ganglion-blocking drug, the ciliary muscle cannot contract (cycloplegia) and the patient loses the ability to focus their eyes. Trimetaphan has a strong effect on the cardiovascular system. The size of blood vessels is primarily controlled by the sympathetic nervous system. Loss of sympathetic system input to the blood vessels causes them to get larger (vasodilation) which has the effect of lowering blood pressure. Postural hypotension is a common side effect of such drugs. Trimethaphan causes a histamine release which further lowers blood pressure. Effects on the heart include a ...
... is an aliphatic, sterically hindered, cyclic, tertiary amine, which is a weak base: in its protonated form it has a pKa of 11.25.[5] Pempidine is a liquid, b.p. 187-188°; d = 0.858 g/cm3.[3] Two early syntheses of this compound are those of Leonard and Hauck,[6] and Hall.[5] These are very similar in principle: Leonard and Hauck reacted phorone with ammonia, to produce 2,2,6,6-tetramethyl-4-piperidone,[7] which was then reduced by means of the Wolff-Kishner reduction to 2,2,6,6-tetramethylpiperidine; this secondary amine was then N-methylated using methyl iodide and potassium carbonate.[8] Hall's method involved reacting acetone with ammonia in the presence of calcium chloride to give 2,2,6,6-tetramethyl-4-piperidone, which was then reduced under Wolff-Kishner conditions, followed by N-methylation of the resulting 2,2,6,6-tetramethylpiperidine with methyl p-toluenesulfonate. ...
Betanidine (or bethanidine) is a sympatholytic drug. Dibenamine (N,N-Dibenzyl-2-chloroethanamine) DE 824208 (1951). ... Phenoxybenzamine B. N. C. Prichard; A. W. Johnston; I. D. Hill & M. L. Rosenheim (1968). "Bethanidine, Guanethidine, and ...
Multicenter Bethanidine Study. Bethanidine sulfate: Efficacy in prevention of ventricular tachyarrhythmias during programmed ... Multicenter Bethanidine Study. / Bethanidine sulfate : Efficacy in prevention of ventricular tachyarrhythmias during programmed ... Multicenter Bethanidine Study (1985). Bethanidine sulfate: Efficacy in prevention of ventricular tachyarrhythmias during ... Multicenter Bethanidine Study 1985, Bethanidine sulfate: Efficacy in prevention of ventricular tachyarrhythmias during ...
Clortermine (Voranil) was developed by Ciba in the 1960s[1] and is an anorectic drug of the amphetamine class.[2] It is the 2-chloro analogue of the better known appetite suppressant phentermine, and is the 2-chloro positional isomer of chlorphentermine. Clortermine produces very low rates of self-administration in animals similarly to chlorphentermine,[3] and as a result it likely does not act on dopamine. Instead, it may act as a serotonin and/or norepinephrine releasing agent.[citation needed] ...
4-Benzylpiperidine is a drug and research chemical used in scientific studies. It acts as a monoamine releasing agent with 20- to 48-fold selectivity for releasing dopamine versus serotonin. It is most efficacious as a releaser of norepinephrine, with an ec50 of 109/41.4/5246nM for DA/NE/5HT, respectively .[1] It has a fast onset of action and a short duration.[1] It also functions as a monoamine oxidase inhibitor (MAOI) with preference for MAO-A.[2] ...
DMA is considered a Schedule 9 prohibited substance in Australia under the Poisons Standard (October 2015).[6] A Schedule 9 substance is a substance which may be abused or misused, the manufacture, possession, sale or use of which should be prohibited by law except when required for medical or scientific research, or for analytical, teaching or training purposes with approval of Commonwealth and/or State or Territory Health Authorities.[6] ...
3,4-Methylenedioxyphenethylamine ("3,4-MDPEA" or just "MDPEA"), also known as homopiperonylamine, is a substituted phenethylamine formed by adding a methylenedioxy group to phenethylamine. It is structurally similar to MDA, but without the methyl group at the alpha position. According to Alexander Shulgin in his book PiHKAL, MDPEA appears to be biologically inactive. This is likely because of extensive first-pass metabolism by the enzyme monoamine oxidase. However, if MDPEA were either used in high enough of doses (e.g., 1-2 grams), or in combination with a monoamine oxidase inhibitor (MAOI), it is probable that it would become sufficiently active, though it would likely have a relatively short duration of action. This idea is similar in concept to the use of selective MAOA inhibitors and selective MAOB inhibitors in augmentation of dimethyltryptamine (DMT) and phenethylamine (PEA), respectively. ...
Alexander Shulgin conducted research on methylenedioxy compounds in the 1960s. In a 1967 lab notebook entry, Shulgin briefly mentioned a colleagues report of no effect from the substance with a 100 mg dose.[4] Shulgin later characterized the substance in his book PiHKAL.[3] In the United States, MDEA was introduced recreationally in 1985 as a legal substitute to the newly banned MDMA.[2] MDEA was made a Schedule 1 substance in the United States on August 13, 1987 under the Federal Analog Act.[1] ...
Hexacyclonate (Gevilon) is a stimulant drug. It has been used for the treatment of alcoholism[1] and for increasing motivation in elderly patients,[2] but is now mainly used for the treatment of hyperlipoproteinaemia. [3][4] It is chemically similar to the anticonvulsant gabapentin, with a hydroxyl group replacing the amine. The latter use may be incorrectly assigned, as "Gevilon" has been used as a trade name for gemfibrozil, a well-known drug for dislypidemia. ...
Difluoromethylenedioxyamphetamine (DiFMDA) is a substituted derivative of 3,4-methylenedioxyamphetamine (MDA), which was developed by Daniel Trachsel and coworkers, along with the corresponding fluorinated derivatives of MDMA, MDEA, BDB and MBDB, with the aim of finding a non-neurotoxic drug able to be used as a less harmful substitute for entactogenic drugs such as MDMA. Since a major route of the normal metabolism of these compounds is scission of the methylenedioxy ring, producing neurotoxic metabolites such as alpha-methyldopamine, it was hoped that the difluoromethylenedioxy bioisostere would show increased metabolic stability and less toxicity.[1][2] These compounds have not yet been tested in animals to verify whether they show similar pharmacological activity to the non-fluorinated parent compounds, although in vitro binding studies show DFMDA to have a SERT affinity in between that of MDA and MDMA.[3] However, there is known to be a lack of bulk tolerance at this position of the ...
Amphetamines like MDMA, MDEA, MDA, and MBDB, among other relatives (see MDxx), are recreational drugs termed entactogens. They act as serotonin-norepinephrine-dopamine releasing agents (SNDRAs) and also agonize serotonin receptors such as those in the 5-HT2 subfamily. Fenfluramine, chlorphentermine, and aminorex, which are also amphetamines and relatives, were formerly used as appetite suppressants but were discontinued due to concerns of cardiac valvulopathy. This side effect has been attributed to their additional action of potent agonism of the 5-HT2B receptor. The designer drug 4-methylaminorex, which is an SNDRA and 5-HT2B agonist, has been reported to cause this effect as well. Many tryptamines, such as DMT, DET, DPT, DiPT, psilocin, and bufotenin, are SRAs as well as non-selective serotonin receptor agonists.[3] These drugs are serotonergic psychedelics, which is a consequence of their ability to activate the 5-HT2A receptor. αET and αMT, also tryptamines, are SNDRAs and non-selective ...
Text is available under the Creative Commons Attribution-ShareAlike License; additional terms may apply. By using this site, you agree to the Terms of Use and Privacy Policy. Wikipedia® is a registered trademark of the Wikimedia Foundation, Inc., a non-profit organization ...
The LD50 for methylhexanamine is 39 mg/kg in mice and 72.5 mg/kg in rats, when administered intravenously.[7]:95[16]:110 The FDA has stated that methylhexanamine "is known to narrow the blood vessels and arteries, which can elevate blood pressure and may lead to cardiovascular events ranging from shortness of breath and tightening in the chest to heart attack".[17] Numerous adverse events and at least five deaths have been reported in association with methylhexanamine-containing dietary supplements.[3] A 2012 review by a panel convened by the U.S. Department of Defense to study whether the military should ban methylhexanamine supplements from stores on its bases concluded that: "The existing evidence does not conclusively establish that DMAA-containing substances are causally-associated with adverse medical events. However, a consistent theme among the studies is that DMAA use potentially affects cardiovascular function, just as other sympathomimetic stimulants. Without further rigorous study ...
Drug discrimination studies showed that 5-methyl-MDA substitutes for MDA, MMAI, and LSD, but not amphetamine, suggesting that it produces a mix of entactogen and hallucinogenic effects without any stimulant effects.[2]. 5-Methyl-MDA acts as a selective serotonin releasing agent (SSRA) with IC50 values of 107nM, 11,600nM, and 1,494nM for serotonin, dopamine, and norepinephrine efflux.[1] It is over 5x more potent than MDA, with a suitable active dose possibly being around 15-25 mg.[1][2] Subsequent testing, however, has found that it is not as potent as once thought and is active at at least 100mg. 2-Methyl-MDA is also much more potent than MDA, but is not quite as potent as 5-methyl-MDA.[1] 6-methyl-MDMA (also known as Madam-6) is mostly inactive, likely due to steric hindrance.[1][3]. Recent research has used data on 2-methyl-MDA and 5-methyl-MDA to help guide computer modeling of the serotonin transporter complex.[4]. ...
The family of drugs typified by MDMA produce their effects through multiple mechanisms of action in the body, and consequently produce three distinct cues which animals can be trained to respond to: a stimulant cue typified by drugs such as methamphetamine, a psychedelic cue typified by drugs such as LSD and DOM, and an "entactogen-like" cue which is produced by drugs such as MDAI and MBDB. These drugs cause drug-appropriate responses in animals trained to recognize the effects of MDMA, but do not produce responses in animals trained selectively to respond to stimulants or hallucinogens. Because these compounds selectively release serotonin in the brain but have little effect on dopamine or noradrenaline levels, they can produce empathogenic effects but without any stimulant action, instead being somewhat sedating.[4][5][6][7][8][9][10] Very high doses can be fatal in rats with a 50% fatality rate for those subcutaneously injected with 28 mg/kg of MDAI. This is a result of the way serotonin ...
Ortetamine (INN), also known as 2-methylamphetamine, is a stimulant drug of the amphetamine class. In animal drug discrimination tests it substituted for dextroamphetamine more closely than either 3- or 4-methylamphetamine, although with only around 1/10 the potency of dextroamphetamine itself.[1] ...
Chlorphentermine (trade names Apsedon, Desopimon, Lucofen) is a serotonergic appetite suppressant of the amphetamine family. Developed in 1962, it is the 4-chloro derivative of the better known appetite suppressant phentermine,[1] which is still in current use. Chlorphentermine acts as a highly selective serotonin releasing agent (SRA).[2] It is not a psychostimulant and has little or no abuse potential, but is classed as a Schedule III drug in the USA due mainly to its similarity to other appetite suppressants such as diethylpropion which have been more widely abused. It is no longer used due mainly to safety concerns, as it has a serotonergic effects profile similar to other withdrawn appetite suppressants such as fenfluramine and aminorex which were found to cause pulmonary hypertension and cardiac fibrosis following prolonged use.[3] The plasma half-life is about five days.[4] It was withdrawn from the market in the UK in 1974.[4] ...
Famprofazone (Gewodin, Gewolen) is a nonsteroidal anti-inflammatory agent (NSAID) of the pyrazolone series which is available over-the-counter in some countries such as Taiwan.[1][2][3] It has analgesic, anti-inflammatory, and antipyretic effects.[1][2] Famprofazone has been known to produce methamphetamine as an active metabolite, with 15-20% of an oral dose being converted to it.[4][5] As a result, famprofazone has occasionally been implicated in causing positives on drug tests for amphetamines.[3] ...
Giugliano D, Luyckx A, Binder D, Lefebvre P. Comparative effects of metformin and indanorex in the treatment of reactive hypoglycemia. International Journal of Clinical Pharmacology and Biopharmacy. 1979 Feb;17(2):76-81. ...
Bethanidine. *Bumetanide (Bumex). *Captopril (Capoten). *Chlorothiazide (Diuril). *Chlorthalidone (Hygroton). *Clonidine ( ...
Schedule H is a class of prescription drugs in India appearing as an appendix to the Drugs and Cosmetics Rules, 1945 introduced in 1945. These are drugs which cannot be purchased over the counter without the prescription of a qualified doctor.The manufacture and sale of all drugs are covered under the Drugs and Cosmetics Act and Rules. It is revised at times based on the advice of the Drugs Technical Advisory Board, part of the Central Drugs Standard Control Organization[1] in the Ministry of Health and Family Welfare. The most recent schedule H (2006) lists 536 drugs from abacavir to zuclopenthixol.[2] However, enforcement of Schedule H laws in India is lax, compared to the more restrictive Schedule X, for which a mandatory documentation trail must be maintained.[3] ...
Detailed drug Information for Norpramin. Includes common brand names, drug descriptions, warnings, side effects and dosing information.
Detailed drug Information for Duo-Vil 2-10. Includes common brand names, drug descriptions, warnings, side effects and dosing information.
bethanidine debrisoquine guanethidine There may be a sudden and marked increase in blood pressure and heart rate when ...
Do not take desipramine with a monoamine oxidase (MAO) inhibitor (eg, isocarboxazid [Marplan®], phenelzine [Nardil®], selegiline [Eldepryl®], tranylcypromine [Parnate®]). Do not start taking desipramine during the 2 weeks after you stop a MAO inhibitor and wait 2 weeks after stopping desipramine before you start taking a MAO inhibitor. If you take them together or do not wait 2 weeks, you may develop confusion, agitation, restlessness, stomach or intestinal symptoms, a sudden high body temperature, an extremely high blood pressure, or severe convulsions. Desipramine may cause a serious condition called serotonin syndrome if taken together with some medicines. Do not use desipramine with buspirone (Buspar®), fentanyl (Abstral®, Duragesic®), linezolid (Zyvox®), lithium (Eskalith®, Lithobid®), methylene blue, tryptophan, St. Johns wort, or some pain or migraine medicines (eg, sumatriptan, tramadol, Frova®, Maxalt®, Relpax®, Zomig®). Check with your doctor first before taking any ...
Phendimetrazine functions as a prodrug to phenmetrazine; approximately 30 percent of an oral dose is converted into it. Phendimetrazine can essentially be thought of as an extended-release formulation of phenmetrazine with less potential for abuse. Phenmetrazine acts as a norepinephrine-dopamine releasing agent (NDRA).[2] Its structure incorporates the backbone of methamphetamine, a potent CNS stimulant. While the addition of an N-methyl group to amphetamine significantly increases its potency and bioavailability, methylation of phendimetrazine renders the compound virtually inactive. Metabolization by demethylases produces a steady, continuous activation of the drug in the body, both lowering abuse potential and allowing for once-daily administration.[citation needed] ...
  • In man, mianserin in therapeutic dosage has no effect on peripheral noradrenaline uptake in the tyramine pressor test, and unlike the tricyclic antidepressants does not significantly decrease the antihypertensive action of bethanidine or guanethidine. (ovid.com)
  • In conclusion, the efficacy of bethanidine for preventing ventricular tachyarrhythmias as assessed by programmed stimulation is low. (elsevier.com)
  • Chronic exposure to an osteopath with no evidence that the expected value is that gps appear to be left in place of measurements made on the first stage of estrous cycle, and in this group, bethanidine and debrisoquine, are now rarely used because of their own cattle. (bigsurlandtrust.org)