Reserpine: An alkaloid found in the roots of Rauwolfia serpentina and R. vomitoria. Reserpine inhibits the uptake of norepinephrine into storage vesicles resulting in depletion of catecholamines and serotonin from central and peripheral axon terminals. It has been used as an antihypertensive and an antipsychotic as well as a research tool, but its adverse effects limit its clinical use.Iproniazid: An irreversible inhibitor of monoamine oxidase types A and B that is used as an antidepressive agent. It has also been used as an antitubercular agent, but its use is limited by its toxicity.Tyramine: An indirect sympathomimetic. Tyramine does not directly activate adrenergic receptors, but it can serve as a substrate for adrenergic uptake systems and monoamine oxidase so it prolongs the actions of adrenergic transmitters. It also provokes transmitter release from adrenergic terminals. Tyramine may be a neurotransmitter in some invertebrate nervous systems.Methyltyrosines: A group of compounds that are methyl derivatives of the amino acid TYROSINE.alpha-Methyltyrosine: An inhibitor of the enzyme TYROSINE 3-MONOOXYGENASE, and consequently of the synthesis of catecholamines. It is used to control the symptoms of excessive sympathetic stimulation in patients with PHEOCHROMOCYTOMA. (Martindale, The Extra Pharmacopoeia, 30th ed)Adrenergic Uptake Inhibitors: Drugs that block the transport of adrenergic transmitters into axon terminals or into storage vesicles within terminals. The tricyclic antidepressants (ANTIDEPRESSIVE AGENTS, TRICYCLIC) and amphetamines are among the therapeutically important drugs that may act via inhibition of adrenergic transport. Many of these drugs also block transport of serotonin.Norepinephrine: Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.Hydroxydopamines: Dopamines with a hydroxy group substituted in one or more positions.Tetrabenazine: A drug formerly used as an antipsychotic and treatment of various movement disorders. Tetrabenazine blocks neurotransmitter uptake into adrenergic storage vesicles and has been used as a high affinity label for the vesicle transport system.Chlorpromazine: The prototypical phenothiazine antipsychotic drug. Like the other drugs in this class chlorpromazine's antipsychotic actions are thought to be due to long-term adaptation by the brain to blocking DOPAMINE RECEPTORS. Chlorpromazine has several other actions and therapeutic uses, including as an antiemetic and in the treatment of intractable hiccup.Mephentermine: A sympathomimetic agent with specificity for alpha-1 adrenergic receptors. It is used to maintain BLOOD PRESSURE in hypotensive states such as following SPINAL ANESTHESIA.Pargyline: A monoamine oxidase inhibitor with antihypertensive properties.Catecholamine Plasma Membrane Transport Proteins: A group of membrane transport proteins that transport biogenic amine derivatives of catechol across the PLASMA MEMBRANE. Catecholamine plasma membrane transporter proteins regulate neural transmission as well as catecholamine metabolism and recycling.Secologanin Tryptamine Alkaloids: Compounds formed by condensation of secologanin with tryptamine resulting in a tetrahydro-beta-carboline which is processed further to a number of bioactive compounds. These are especially found in plants of the APOCYNACEAE; LOGANIACEAE; and RUBIACEAE families.Catecholamines: A general class of ortho-dihydroxyphenylalkylamines derived from tyrosine.Biogenic Amines: A group of naturally occurring amines derived by enzymatic decarboxylation of the natural amino acids. Many have powerful physiological effects (e.g., histamine, serotonin, epinephrine, tyramine). Those derived from aromatic amino acids, and also their synthetic analogs (e.g., amphetamine), are of use in pharmacology.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.Nialamide: An MAO inhibitor that is used as an antidepressive agent.Adrenal Medulla: The inner portion of the adrenal gland. Derived from ECTODERM, adrenal medulla consists mainly of CHROMAFFIN CELLS that produces and stores a number of NEUROTRANSMITTERS, mainly adrenaline (EPINEPHRINE) and NOREPINEPHRINE. The activity of the adrenal medulla is regulated by the SYMPATHETIC NERVOUS SYSTEM.Vesicular Monoamine Transport Proteins: A family of vesicular amine transporter proteins that catalyze the transport and storage of CATECHOLAMINES and indolamines into SECRETORY VESICLES.Pituitary Irradiation: Radiation therapy used to treat the PITUITARY GLAND.Bretylium CompoundsVesicular Biogenic Amine Transport Proteins: Integral membrane proteins of the LIPID BILAYER of SECRETORY VESICLES that catalyze transport and storage of biogenic amine NEUROTRANSMITTERS such as ACETYLCHOLINE; SEROTONIN; MELATONIN; HISTAMINE; and CATECHOLAMINES. The transporters exchange vesicular protons for cytoplasmic neurotransmitters.Serotonin: A biochemical messenger and regulator, synthesized from the essential amino acid L-TRYPTOPHAN. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (RECEPTORS, SEROTONIN) explain the broad physiological actions and distribution of this biochemical mediator.Normetanephrine: A methylated metabolite of norepinephrine that is excreted in the urine and found in certain tissues. It is a marker for tumors.Fenclonine: A selective and irreversible inhibitor of tryptophan hydroxylase, a rate-limiting enzyme in the biosynthesis of serotonin (5-HYDROXYTRYPTAMINE). Fenclonine acts pharmacologically to deplete endogenous levels of serotonin.Chromaffin Granules: Organelles in CHROMAFFIN CELLS located in the adrenal glands and various other organs. These granules are the site of the synthesis, storage, metabolism, and secretion of EPINEPHRINE and NOREPINEPHRINE.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)17-Hydroxycorticosteroids: A group of hydroxycorticosteroids bearing a hydroxy group at the 17-position. Urinary excretion of these compounds is used as an index of adrenal function. They are used systemically in the free alcohol form, but with esterification of the hydroxy groups, topical effectiveness is increased.Methyldopa: An alpha-2 adrenergic agonist that has both central and peripheral nervous system effects. Its primary clinical use is as an antihypertensive agent.Pharmacology: The study of the origin, nature, properties, and actions of drugs and their effects on living organisms.Phenoxybenzamine: An alpha-adrenergic antagonist with long duration of action. It has been used to treat hypertension and as a peripheral vasodilator.Synephrine: Sympathetic alpha-adrenergic agonist with actions like PHENYLEPHRINE. It is used as a vasoconstrictor in circulatory failure, asthma, nasal congestion, and glaucoma.Methysergide: An ergot derivative that is a congener of LYSERGIC ACID DIETHYLAMIDE. It antagonizes the effects of serotonin in blood vessels and gastrointestinal smooth muscle, but has few of the properties of other ergot alkaloids. Methysergide is used prophylactically in migraine and other vascular headaches and to antagonize serotonin in the carcinoid syndrome.Dopamine: One of the catecholamine NEUROTRANSMITTERS in the brain. It is derived from TYROSINE and is the precursor to NOREPINEPHRINE and EPINEPHRINE. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of receptors (RECEPTORS, DOPAMINE) mediate its action.Chromaffin System: The cells of the body which stain with chromium salts. They occur along the sympathetic nerves, in the adrenal gland, and in various other organs.Clopamide: A sulfamoylbenzamide piperidine. It is considered a thiazide-like diuretic.Vas Deferens: The excretory duct of the testes that carries SPERMATOZOA. It rises from the SCROTUM and joins the SEMINAL VESICLES to form the ejaculatory duct.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)Chlorisondamine: A nicotinic antagonist used primarily as a ganglionic blocker in animal research. It has been used as an antihypertensive agent but has been supplanted by more specific drugs in most clinical applications.Tranquilizing Agents: A traditional grouping of drugs said to have a soothing or calming effect on mood, thought, or behavior. Included here are the ANTI-ANXIETY AGENTS (minor tranquilizers), ANTIMANIC AGENTS, and the ANTIPSYCHOTIC AGENTS (major tranquilizers). These drugs act by different mechanisms and are used for different therapeutic purposes.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.Desipramine: A tricyclic dibenzazepine compound that potentiates neurotransmission. Desipramine selectively blocks reuptake of norepinephrine from the neural synapse, and also appears to impair serotonin transport. This compound also possesses minor anticholinergic activity, through its affinity to muscarinic receptors.5-Hydroxytryptophan: The immediate precursor in the biosynthesis of SEROTONIN from tryptophan. It is used as an antiepileptic and antidepressant.Dextroamphetamine: The d-form of AMPHETAMINE. It is a central nervous system stimulant and a sympathomimetic. It has also been used in the treatment of narcolepsy and of attention deficit disorders and hyperactivity in children. Dextroamphetamine has multiple mechanisms of action including blocking uptake of adrenergics and dopamine, stimulating release of monamines, and inhibiting monoamine oxidase. It is also a drug of abuse and a psychotomimetic.Ephedrine: A phenethylamine found in EPHEDRA SINICA. PSEUDOEPHEDRINE is an isomer. It is an alpha- and beta-adrenergic agonist that may also enhance release of norepinephrine. It has been used for asthma, heart failure, rhinitis, and urinary incontinence, and for its central nervous system stimulatory effects in the treatment of narcolepsy and depression. It has become less extensively used with the advent of more selective agonists.Metaraminol: A sympathomimetic agent that acts predominantly at alpha-1 adrenergic receptors. It has been used primarily as a vasoconstrictor in the treatment of HYPOTENSION.Epinephrine: The active sympathomimetic hormone from the ADRENAL MEDULLA. It stimulates both the alpha- and beta- adrenergic systems, causes systemic VASOCONSTRICTION and gastrointestinal relaxation, stimulates the HEART, and dilates BRONCHI and cerebral vessels. It is used in ASTHMA and CARDIAC FAILURE and to delay absorption of local ANESTHETICS.Dihydroxyphenylalanine: A beta-hydroxylated derivative of phenylalanine. The D-form of dihydroxyphenylalanine has less physiologic activity than the L-form and is commonly used experimentally to determine whether the pharmacological effects of LEVODOPA are stereospecific.Adrenergic Agents: Drugs that act on adrenergic receptors or affect the life cycle of adrenergic transmitters. Included here are adrenergic agonists and antagonists and agents that affect the synthesis, storage, uptake, metabolism, or release of adrenergic transmitters.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)Biogenic Monoamines: Biogenic amines having only one amine moiety. Included in this group are all natural monoamines formed by the enzymatic decarboxylation of natural amino acids.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 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.Indole Alkaloids: Group of alkaloids containing a benzylpyrrole group (derived from TRYPTOPHAN)

Influence of vesicular storage and monoamine oxidase activity on [11C]phenylephrine kinetics: studies in isolated rat heart. (1/855)

[11C]Phenylephrine (PHEN) is a radiolabeled analogue of norepinephrine that is transported into cardiac sympathetic nerve varicosities by the neuronal norepinephrine transporter and taken up into storage vesicles localized within the nerve varicosities by the vesicular monoamine transporter. PHEN is structurally related to two previously developed sympathetic nerve markers: [11C]-meta-hydroxyephedrine and [11C]epinephrine. To better characterize the neuronal handling of PHEN, particularly its sensitivity to neuronal monoamine oxidase (MAO) activity, kinetic studies in an isolated working rat heart system were performed. METHODS: Radiotracer was administered to the isolated working heart as a 10-min constant infusion followed by a 110-min washout period. Two distinctly different approaches were used to assess the sensitivity of the kinetics of PHEN to MAO activity. In the first approach, oxidation of PHEN by MAO was inhibited at the enzymatic level with the MAO inhibitor pargyline. In the second approach, the two hydrogen atoms on the a-carbon of the side chain of PHEN were replaced with deuterium atoms ([11C](-)-alpha-alpha-dideutero-phenylephrine [D2-PHEN]) to inhibit MAO activity at the tracer level. The importance of vesicular uptake on the kinetics of PHEN and D2-PHEN was assessed by inhibiting vesicular monoamine transporter-mediated storage into vesicles with reserpine. RESULTS: Under control conditions, PHEN initially accumulated into the heart at a rate of 0.72+/-0.15 mL/min/g wet. Inhibition of MAO activity with either pargyline or di-deuterium substitution did not significantly alter this rate. However, MAO inhibition did significantly slow the clearance of radioactivity from the heart during the washout phase of the study. Blocking vesicular uptake with reserpine reduced the initial uptake rates of PHEN and D2-PHEN, as well as greatly accelerated the clearance of radioactivity from the heart during washout. CONCLUSION: These studies indicate that PHEN kinetics are sensitive to neuronal MAO activity. Under normal conditions, efficient vesicular storage of PHEN serves to protect the tracer from rapid metabolism by neuronal MAO. However, it is likely that leakage of PHEN from the storage vesicles and subsequent metabolism by MAO lead to an appreciable clearance of radioactivity from the heart.  (+info)

Influence of a new antiulcer agent, ammonium 7-oxobicyclo (2, 2, 1) hept-5-ene-3-carbamoyl-2-carboxylate (KF-392) on gastric lesions and gastric mucosal barrier in rats. (2/855)

Antiulcer effects of KF-392 were studied in several experimental gastric ulcer models in rats. It was found that KF-392 given orally at 1.0 to 5.0 mg/kg had a marked suppression on the developments of Shay ulcer as well as the aspirin-, stress-, and reserpine-induced gastric lesions. The influence of KF-392 on gastric mucosal barrier was also studied. A back diffusion of H+ into the gastric mucosa and a fall of transmucosal potential difference were induced with KF-392 given orally at the above mentioned doses. KF-392 given s.c. at 5.0 mg/kg showed no inhibition of Shay ulcer and no induction of back diffusion of H+ into the gastric mucosa.  (+info)

A possible mode of cardiovascular actions of dopamine in dogs. (3/855)

A possible mode of cardiovascular actions of dopamine was studied using ephedrine. In the dog pretreated with repeated administrations of ephedrine (total dose, 40 or 80 mg/kg, i.v.) or with combined administrations of ephedrine (total dose, 90 mg/kg, s.c. and i.v.) and reserpine (2 mg/kg, s.c., 24 hr previously), pressor responses to dopamine were eliminated and reversed to depressor responses whereas depressor responses to dopamine were potentiated. Positive chronotropic effects of dopamine were almost eliminated. Pressor and positive chronotropic effects of tyramine were almost abolished. Sympathomimetic effect of noradrenaline and adrenaline were potentiated while those of isoprenaline were inhibited. In the heart-lung preparation of ephedrine-treated dogs (total dose, 40 mg/kg, i.v.), cardiac stimulating effects of dopamine and tyramine were strongly depressed, and those of noradrenaline, adrenaline and isoprenaline were reduced to some extent. In the open-chest dogs, after pretreatment of cocaine (4 mg/kg, i.v.), pressor, positive inotropic and chronotropic effects of noradrenaline were potentiated, whilst those of tyramine were inhibited. Those of dopamine were not visibly altered, but depressor, negative chronotropic and inotropic effects of dopamine appeared at small doses. In the ephedrine-pretreated dogs, these sympathomimetic effects of dopamine and tyramine after cocaine were strongly depressed and those of noradrenaline were inhibited to a certain degree. The results obtained with ephedrine suggest that dopamine differs from other catecholamines and tyramine in the mode of cardiovascular actions.  (+info)

Pharmacodynamic actions of (S)-2-[4,5-dihydro-5-propyl-2-(3H)-furylidene]-1,3-cyclopentanedione (oudenone). (4/855)

The pharmacodynamic actions of (S)-2-[4,5-dihydro-5-propyl-2(3H)-furylidene]-1,3-cyclopentanedione (oudenone) were studied in both anesthetized animals and isolated organs. Oudenone (10--40 mg/kg i.v.) induced an initial rise in blood pressure followed by a prolonged hypotension in the anesthetized rats. In unanesthetized spontaneously hypertensive rats (SHR), oudenone (5--200 mg/kg p.o.) caused a dose-related decrease in the systolic blood pressure. The initial pressor effect was diminished by pretreatments with phentolamine, guanethidine, hexamethonium and was abolished in the pithed rats. In addition, intracisternal administrations of oudenone (100--600 mug/kg) showed a marked increase in blood pressure in the anesthetized rats, suggesting that the pressor effect may be due to centrally mediated actions. Oudenone, given intra-arterially into the femoral artery (400--800 mug/kg), caused a long-lasting vasodilation in anesthetized dogs. At a relatively high dose (40 mg/kg i.v.), oudenone antagonized all pressor responses to autonomic agents and central vagus nerve stimulation in anesthetized rats and dogs, however, oudenone showed no anti-cholinergic,-histaminergic, beta-adrenergic and adrenergic neuron blocking properties.  (+info)

The role of the sympathetic nervous system in the regulation of leptin synthesis in C57BL/6 mice. (5/855)

The objectives of this study were to determine whether leptin synthesis is regulated by the sympathetic nervous system and if so whether beta-adrenergic receptors mediate this effect. We show that sympathetic blockade by reserpine increases leptin mRNA levels in brown but not white adipose tissue, while acute cold-exposure decreases leptin expression 10-fold in brown adipose tissue and 2-fold in white adipose tissue. The cold-induced reduction in leptin mRNA can be prevented by a combination of propranolol and SR 59230A but not by either antagonist alone, indicating that beta3-adrenergic receptors and classical beta1/beta2-adrenergic receptors both mediate responses to sympathetic stimulation. Circulating leptin levels reflect synthesis in white adipose tissue but not in brown adipose tissue.  (+info)

The effect of reserpine, an inhibitor of multidrug efflux pumps, on the in-vitro activities of ciprofloxacin, sparfloxacin and moxifloxacin against clinical isolates of Staphylococcus aureus. (6/855)

In Staphylococcus aureus, in addition to mutations in the grl and gyr gene loci, multidrug efflux pumps like NorA contribute to decreased fluoroquinolone susceptibility. Efflux pumps can be inhibited by the plant alkaloid reserpine, which, at 20 mg/L, reduced sparfloxacin, moxifloxacin and ciprofloxacin IC50s and MICs by up to four-fold in 11, 21 and 48 of the 102 unrelated clinical isolates tested, respectively. The effect was less pronounced with the hydrophobic drugs sparfloxacin and moxifloxacin than with the hydrophilic drug ciprofloxacin and was stable in all 25 clonally related isolates tested.  (+info)

Increased methamphetamine neurotoxicity in heterozygous vesicular monoamine transporter 2 knock-out mice. (7/855)

Methamphetamine (METH) is a powerful psychostimulant that is increasingly abused worldwide. Although it is commonly accepted that the dopaminergic system and oxidation of dopamine (DA) play pivotal roles in the neurotoxicity produced by this phenylethylamine, the primary source of DA responsible for this effect has remained elusive. In this study, we used mice heterozygous for vesicular monoamine transporter 2 (VMAT2 +/- mice) to determine whether impaired vesicular function alters the effects of METH. METH-induced dopaminergic neurotoxicity was increased in striatum of VMAT2 +/- mice compared with wild-type mice as revealed by a more consistent DA and metabolite depletion and a greater decrease in dopamine transporter expression. Interestingly, increased METH neurotoxicity in VMAT2 +/- mice was accompanied by less pronounced increase in extracellular DA and indices of free radical formation compared with wild-type mice. These results indicate that disruption of vesicular monoamine transport potentiates METH-induced neurotoxicity in vivo and point, albeit indirectly, to a greater contribution of intraneuronal DA redistribution rather than extraneuronal overflow on mediating this effect.  (+info)

Inhibition of the emergence of ciprofloxacin resistance in Streptococcus pneumoniae by the multidrug efflux inhibitor reserpine. (8/855)

Recent evidence supports the contribution of a multidrug efflux mechanism to fluoroquinolone resistance in Streptococcus pneumoniae. In this paper I show that reserpine, an inhibitor of multidrug transporters in gram-positive bacteria, dramatically suppresses the in vitro emergence of ciprofloxacin-resistant variants of S. pneumoniae, suggesting that the combination of a fluoroquinolone with an inhibitor of multidrug transport may help preserve the efficacy of this class of antibiotics.  (+info)

  • Reserpine-mediated depletion of monoamine neurotransmitters in the synapses is often cited as evidence to the theory that depletion of the monoamine neurotransmitters causes subsequent depression in humans (c.f. monoamine hypothesis). (
  • The akinetic state, resulting from reserpine-induced dopamine depletion in the caudate nucleus and putamen, led Carlsson to speculate that PD was due to loss of dopamine neurotransmission. (
  • 1. Reserpine (5 mg/kg intraperitoneally) produced gastric mucosal vasoconstriction and injury in all rats within 6 h (injury score 38.8 ± 2.1 mm 2 , mean ± SEM). (
  • 3. The results suggest that, in the rat, reserpine causes vagal α-adrenoceptor stimulation producing gastric mucosal vasoconstriction and injury. (
  • Protective effect of centrally-injected glucagon-like peptide-1 on reserpine-induced gastric mucosal lesions in rat: possible mechanisms. (
  • After 2 h of 18 F-LMI1195 preloading into both cell lines, effects of stimulants for storage vesicle turnover (high concentration KCl (100 mM) or reserpine treatment) were measured at 10, 20, and 30 min. (
  • Both high concentration KCl and reserpine enhanced 18 F-LMI1195 washout from PC12 cells, while tracer retention remained stable in the SK-N-SH cells. (
  • You should not use reserpine if you have a stomach ulcer, ulcerative colitis, a history of depression or suicidal thoughts, or if you are being treated with electroconvulsive therapy. (
  • Coeliac ganglionectomy or the β-adrenoceptor-blocking drug propranolol (5-15 mg/kg) did not influence these effects of reserpine, but vagotomy protected the rats against them. (
  • Measurements of reserpine in the brain of normal and tetrabenazine-pretreated rats supply direct evidence in favor of the view that these drugs compete at the level of a common target. (
  • Manara, L & Garattini, S 1967, ' Time course of 3H-reserpine levels in brains of normal and tetrabenazine-pretreated rats ', European Journal of Pharmacology , vol. 2, no. 2, pp. 139-141. (
  • Reserpine was isolated in 1952 from the dried root of Rauwolfia serpentina (Indian snakeroot), which had been known as Sarpagandha and had been used for centuries in India for the treatment of insanity, as well as fever and snakebites - Mahatma Gandhi used it as a tranquilizer. (
  • Similar tracer kinetics after KCl or reserpine treatment were also observed using 131 I-MIBG. (
  • Tryptophan is the starting material in the biosynthetic pathway of reserpine, and is converted to tryptamine by tryptophan decarboxylase enzyme. (
  • The first demonstration of an animal model for PD was reported by Carlsson in the 1950s using rabbits treated with reserpine. (
  • Moreover, reserpine has a peripheral action in many parts of the body, resulting in a preponderance of the effects of the cholinergic part of the autonomous nervous system on the GI tract, smooth muscles, blood vessels, etc. (
  • The reserpine-induced depression is considered by some researchers to be a myth, while others claim that teas made out of the plant roots containing reserpine have a calming, sedative action that can actually be considered antidepressant. (
  • Reserpine was also highly influential in promoting the thought of a biogenic amine hypothesis of depression - see Everett & Tolman, 1959. (
  • Some people taking reserpine have developed depression. (
  • Notably, reserpine was the first compound shown to be an effective antidepressant in a randomized placebo-controlled trial. (
  • In addition the results of the present drug interaction study underline the relevance of the long-lasting concentrations of reserpine in the brain for explaining the functional modifications induced by its administration. (
  • If you need surgery, tell the surgeon ahead of time that you are using reserpine. (
  • Labarthe, DR & O'Fallon, WM 1977, ' Reserpine and breast cancer: A longitudinal study of over 2000 hypertensive women ', American Journal of Epidemiology , vol. 106, no. 3. (
  • U'Prichard, DC & Snyder, SH 1978, ' 3H-catecholamine binding to α-receptors in rat brain: Enhancement by reserpine ', European Journal of Pharmacology , vol. 51, no. 2, pp. 145-155. (
  • If you become pregnant while taking reserpine, call your doctor. (
  • Tell your doctor if you are pregnant or plan to become pregnant while taking reserpine. (
  • Finally, cotransfer experiments indicated that the effect of reserpine on the transfer of CS was not due to activation of suppressor cells. (
  • Kalueff, A. V. Behavioral effects of bidirectional modulators of brain monoamines reserpine and d-amphetamine in zebrafish. (
  • Reserpine precludes the storage of monoamines through the blockage of the synaptic vesicles transporters [ 1 ]. (
  • Besides its classical mechanism of action (i.e. blockage of the vesicular transport of monoamines), there is clear evidence that reserpine also causes an increase in cellular oxidative stress, possibly potentiated by the rise in the levels of dopamine in the cytoplasm, which undergoes oxidative metabolism [ 10 ]. (
  • Reserpine acts at the membrane of intraneuronal granules which store monoamines (NA, 5-HT, DA) and irreversibly inhibits the active amine transporters so the monoamines are gradually depleted and degraded by MAO. (
  • Reserpine is a catecholamine-depleting agent that blocks vesicular storage of monoamines. (
  • A structure-function relationship among reserpine and yohimbine analogues in their ability to increase expression of mdr1 and P-glycoprotein in a human colon carcinoma cell line. (
  • We previously showed that there is a structure-function relationship among reserpine and yohimbine analogues in their ability to inhibit the function of P-glycoprotein (P-gp) and reverse multidrug resistance (MDR). (
  • Because some P-gp inhibitors (e.g., verapamil and nifedipine) can increase mdr1 and P-gp expression in human colon carcinoma cell lines, we used our reserpine/yohimbine analogues to determine whether there was a structural requirement for this induction. (
  • The reserpine/yohimbine analogues rescinnamine, trimethoxybenzoylyohimbine, and LY191401 (compound G), all of which contain the three structural elements used to describe the MDR pharmacophore, also increased both mdr1 and P-gp expression significantly. (
  • The daily dose of reserpine in antihypertensive treatment is as low as 0.1 to 0.25 mg. (
  • Reserpine (0.25 mg/kg s.c. per day for 3 weeks) causes 25 and 46% increases in the numbers of (±)- 3 H-epinephrine and 3 H-WB-4101 α-receptor binding sites respectively, and a 51% increase in the number of 3 H-dihydroalprenolol β-receptor sites, in rat forebrain. (
  • Reserpine (0.25 mg/kg s.c. per day for 3 weeks) causes 25 and 46{\%} increases in the numbers of (±)-3H-epinephrine and 3H-WB-4101 α-receptor binding sites respectively, and a 51{\%} increase in the number of 3H-dihydroalprenolol β-receptor sites, in rat forebrain. (
  • Reserpine (Lannett's Serpalan) is an indole alkaloid antipsychotic and antihypertensive drug that has been used for the control of high blood pressure and for the relief of psychotic symptoms. (
  • Reserpine is an indole alkaloid isolated in 1952 from the extract of Rauwolfia sepentina or 'Indian snake root', a popular plant in traditional Indian medicine used as a sedative and antipyretic, and reportedly taken by Mahatma Gandhi himself. (
  • Reserpine, an indole alkaloid and antipsychotic drug, is used to control high blood pressure and to relieve psychotic symptoms. (
  • The finding that reserpine-induced oral dyskinesia persisted despite repletion of dopamine in the caudate-putamen suggests that the persistent neuropathological change underlying this behavior occurs in a neural pathway other than the dopaminergic nigrostriatal pathway. (
  • Serpalan etc. (reserpine) is an anti-adrenergic medication used to treat high blood pressure (hypotension). (
  • The animals treated with reserpine showed moderate alterations at hind limb skeletal muscles level and had difficulty in moving, together with significant morphological and ultrastructural alterations and expression of inflammatory and oxidative stress markers in the gastrocnemius muscle. (
  • In the biochemical level, the ability of astaxanthin to mitigate reserpine-induced oxidative stress was evaluated by the measurement of malondialdehyde (MDA) and nitric oxide (NO) in brain, liver and plasma samples. (
  • Conclusion: This study suggests that astaxanthin reduces reserpine-induced oxidative stress and therefore might be effective in treating oxidative stress associated depression. (
  • in order to investigate a possible role of nigrostriatal dopaminergic supersensitivity and of oxidative stress in aging- and reserpine-induced OD, the stereotyped behavior induced by dopaminergic agonists, a functional index of dopaminergic striatal activity, as well as the striatal antioxidant enzymes glutathione peroxidase and catalase were assessed. (
  • The increase in enzyme activity of rat ganglia and adrenals was dose-dependent up to 5 mg/kg and persisted for at least four days after reserpine was given. (
  • You may require a lower dose or special monitoring during therapy with chlorothiazide and reserpine if you have any of the conditions listed above. (
  • What is the most important information I should know about chlorothiazide and reserpine?Stand up slowly from a sitting or lying position. (
  • Reserpine may also be used for purposes not listed in this medication guide. (
  • Reserpine used in conjunction with other psychotropic medication may be considered in the treatment of refractory mania, but controlled trials are necessary to support our finding more generally. (
  • The Medication Drug Savings card saves you up to 85% or more on Reserpine and Chlorthalidone . (
  • Reserpine was isolated in 1952 from the dried root of Rauwolfia serpentina (Indian snakeroot), which had been known as Sarpagandha and had been used for centuries in India for the treatment of insanity, as well as fever and snakebites - Mahatma Gandhi used it as a tranquilizer. (
  • reserpine rĕsûr´pēn [ key ] , alkaloid isolated from the root of the snakeroot plant ( Rauwolfia serpentina ), a small evergreen climbing shrub of the dogbane family native to the Indian subcontinent. (
  • Although there is no specific information comparing use of reserpine, hydralazine, and hydrochlorothiazide combination in the elderly with use in other age groups, this medicine is not expected to cause different side effects or problems in older people than it does in younger adults. (
  • Since reserpine increases gastrointestinal motility and secretion, it should be used cautiously in patients with a history of peptic ulcer , ulcerative colitis , or gallstones ( biliary colic may be precipitated). (
  • After the administration of reserpine, the in vitro tyrosine hydroxylase activity increases in rat, guinea-pig, mouse and rabbit adrenal gland, in rat superior cervical ganglia and in rabbit brainstem. (
  • Reserpine controls high blood pressure or symptoms of agitation, but does not cure them. (
  • His manic symptoms improved markedly with the addition of reserpine to the treatment regimen. (
  • Reserpine is a kind of drug that is being used for the control of high blood pressure and for the relief of psychotic symptoms. (
  • The results show a preventive role of alpha-tocopherol on behavioral alterations induced by repeated reserpine treatment. (
  • Method: On the behavioral level, antidepressant property of astaxanthin (50 mg/kg, orally) on reserpine (2 mg/kg, subcutaneously) induced depressed mice was evaluated by forced swim test (FST) and tail suspension test (TST). (
  • tell your doctor and pharmacist if you are allergic to reserpine, aspirin, any other medications, tartrazine (a yellow dye in some processed foods and medications), or any of the ingredients in reserpine tablets. (
  • Reserpine is used to treat high blood pressure. (
  • If you suddenly stop taking reserpine you may develop high blood pressure and experience unwanted side effects. (
  • Rauvolfia (family Apocynaceae ) A genus of shrubs or small trees, some species of which, especially R. serpentina , produce the alkaloid reserpine, used to counteract high blood pressure. (
  • Together, chlorthalidone and reserpine are used to lower high blood pressure. (
  • Orally administered reserpine is readily absorbed from the GI tract. (
  • There is a report of galactorrhea associated with reserpine. (
  • Reserpine has reportedly caused galactorrhea and has been used to increase breastmilk production, although it is obsolete for this use. (
  • In addition the results of the present drug interaction study underline the relevance of the long-lasting concentrations of reserpine in the brain for explaining the functional modifications induced by its administration. (
  • Because an important loss of dopaminergic neurons is the core feature of Parkinson´s disease (PD) [ 2 ], reserpine administration to rodents is a valid approach to study this disease in animal models [ 3 - 5 ]. (
  • Jacobsen, E. N. Enantioselective Total Synthesis of (+)-Reserpine. (