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.
Substances that contain a fused three-ring moiety and are used in the treatment of depression. These drugs block the uptake of norepinephrine and serotonin into axon terminals and may block some subtypes of serotonin, adrenergic, and histamine receptors. However the mechanism of their antidepressant effects is not clear because the therapeutic effects usually take weeks to develop and may reflect compensatory changes in the central nervous system.
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.
The prototypical tricyclic antidepressant. It has been used in major depression, dysthymia, bipolar depression, attention-deficit disorders, agoraphobia, and panic disorders. It has less sedative effect than some other members of this therapeutic group.
Mood-stimulating drugs used primarily in the treatment of affective disorders and related conditions. Several MONOAMINE OXIDASE INHIBITORS are useful as antidepressants apparently as a long-term consequence of their modulation of catecholamine levels. The tricyclic compounds useful as antidepressive agents (ANTIDEPRESSIVE AGENTS, TRICYCLIC) also appear to act through brain catecholamine systems. A third group (ANTIDEPRESSIVE AGENTS, SECOND-GENERATION) is a diverse group of drugs including some that act specifically on serotonergic systems.
The first highly specific serotonin uptake inhibitor. It is used as an antidepressant and often has a more acceptable side-effects profile than traditional antidepressants.
A tricyclic antidepressant similar to IMIPRAMINE that selectively inhibits the uptake of serotonin in the brain. It is readily absorbed from the gastrointestinal tract and demethylated in the liver to form its primary active metabolite, desmethylclomipramine.
Sodium chloride-dependent neurotransmitter symporters located primarily on the PLASMA MEMBRANE of noradrenergic neurons. They remove NOREPINEPHRINE from the EXTRACELLULAR SPACE by high affinity reuptake into PRESYNAPTIC TERMINALS. It regulates signal amplitude and duration at noradrenergic synapses and is the target of ADRENERGIC UPTAKE INHIBITORS.
Tricyclic antidepressant similar in action and side effects to IMIPRAMINE. It may produce excitation.
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.
Tricyclic antidepressant with anticholinergic and sedative properties. It appears to prevent the re-uptake of norepinephrine and serotonin at nerve terminals, thus potentiating the action of these neurotransmitters. Amitriptyline also appears to antagonize cholinergic and alpha-1 adrenergic responses to bioactive amines.
A bridged-ring tetracyclic antidepressant that is both mechanistically and functionally similar to the tricyclic antidepressants, including side effects associated with its use.
A selective serotonin reuptake inhibitor that is used in the treatment of DEPRESSION and a variety of ANXIETY DISORDERS.
A subclass of alpha-adrenergic receptors found on both presynaptic and postsynaptic membranes where they signal through Gi-Go G-PROTEINS. While postsynaptic alpha-2 receptors play a traditional role in mediating the effects of ADRENERGIC AGONISTS, the subset of alpha-2 receptors found on presynaptic membranes signal the feedback inhibition of NEUROTRANSMITTER release.
A tetracyclic compound with antidepressant effects. It may cause drowsiness and hematological problems. Its mechanism of therapeutic action is not well understood, although it apparently blocks alpha-adrenergic, histamine H1, and some types of serotonin receptors.
Compounds with two BENZENE rings fused to AZEPINES.
A metabolite of AMITRIPTYLINE that is also used as an antidepressive agent. Nortriptyline is used in major depression, dysthymia, and atypical depressions.
A suspected industrial carcinogen (and listed as such by OSHA). Its N-hydroxy metabolite is strongly carcinogenic and mutagenic.
An isoquinoline derivative that prevents dopamine reuptake into synaptosomes. The maleate was formerly used in the treatment of depression. It was withdrawn worldwide in 1986 due to the risk of acute hemolytic anemia with intravascular hemolysis resulting from its use. In some cases, renal failure also developed. (From Martindale, The Extra Pharmacopoeia, 30th ed, p266)
A quinolizidine alkaloid isolated from several FABACEAE including LUPINUS; SPARTIUM; and CYTISUS. It has been used as an oxytocic and an anti-arrhythmia agent. It has also been of interest as an indicator of CYP2D6 genotype.
An activity in which the body is propelled through water by specific movement of the arms and/or the legs. Swimming as propulsion through water by the movement of limbs, tail, or fins of animals is often studied as a form of PHYSICAL EXERTION or endurance.
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.
Tryptamine substituted with two hydroxyl groups in positions 5 and 7. It is a neurotoxic serotonin analog that destroys serotonergic neurons preferentially and is used in neuropharmacology as a tool.
Hallucinogenic alkaloid isolated from the flowering heads (peyote) of Lophophora (formerly Anhalonium) williamsii, a Mexican cactus used in Indian religious rites and as an experimental psychotomimetic. Among its cellular effects are agonist actions at some types of serotonin receptors. It has no accepted therapeutic uses although it is legal for religious use by members of the Native American Church.
One of the SEROTONIN UPTAKE INHIBITORS formerly used for depression but was withdrawn worldwide in September 1983 because of the risk of GUILLAIN-BARRE SYNDROME associated with its use. (From Martindale, The Extra Pharmacopoeia, 29th ed, p385)
An imidazoline sympatholytic agent that stimulates ALPHA-2 ADRENERGIC RECEPTORS and central IMIDAZOLINE RECEPTORS. It is commonly used in the management of HYPERTENSION.
A serotonin uptake inhibitor that is effective in the treatment of depression.
Compounds that specifically inhibit the reuptake of serotonin in the brain.
A sympathomimetic agent that acts predominantly at alpha-1 adrenergic receptors. It has been used primarily as a vasoconstrictor in the treatment of HYPOTENSION.
The action of a drug that may affect the activity, metabolism, or toxicity of another drug.
A methylated metabolite of norepinephrine that is excreted in the urine and found in certain tissues. It is a marker for tumors.
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.
A structurally and mechanistically diverse group of drugs that are not tricyclics or monoamine oxidase inhibitors. The most clinically important appear to act selectively on serotonergic systems, especially by inhibiting serotonin reuptake.
A monoamine oxidase inhibitor with antihypertensive properties.
Monohydroxy derivatives of cyclohexanes that contain the general formula R-C6H11O. They have a camphorlike odor and are used in making soaps, insecticides, germicides, dry cleaning, and plasticizers.
An enzyme that catalyzes the hydrolysis of a ceramidetrihexoside to a ceramidedihexoside plus galactose.
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.
A selective serotonin uptake inhibitor that is used in the treatment of depression.
One of the MONOAMINE OXIDASE INHIBITORS used to treat DEPRESSION; PHOBIC DISORDERS; and PANIC.
Drugs that inhibit the transport of neurotransmitters into axon terminals or into storage vesicles within terminals. For many transmitters, uptake determines the time course of transmitter action so inhibiting uptake prolongs the activity of the transmitter. Blocking uptake may also deplete available transmitter stores. Many clinically important drugs are uptake inhibitors although the indirect reactions of the brain rather than the acute block of uptake itself is often responsible for the therapeutic effects.
An alpha-1 adrenergic agonist that causes prolonged peripheral VASOCONSTRICTION.
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)
Neurons whose primary neurotransmitter is EPINEPHRINE.
A cytochrome P450 enzyme that catalyzes the hydroxylation of many drugs and environmental chemicals, such as DEBRISOQUINE; ADRENERGIC RECEPTOR ANTAGONISTS; and TRICYCLIC ANTIDEPRESSANTS. This enzyme is deficient in up to 10 percent of the Caucasian population.
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.
Biogenic amines having only one amine moiety. Included in this group are all natural monoamines formed by the enzymatic decarboxylation of natural amino acids.
An antidepressive agent and monoamine oxidase inhibitor related to PARGYLINE.
A group of compounds that are methyl derivatives of the amino acid TYROSINE.
Services providing pharmaceutic and therapeutic drug information and consultation.
Printed publications usually having a format with no binding and no cover and having fewer than some set number of pages. They are often devoted to a single subject.
Use of written, printed, or graphic materials upon or accompanying a drug container or wrapper. It includes contents, indications, effects, dosages, routes, methods, frequency and duration of administration, warnings, hazards, contraindications, side effects, precautions, and other relevant information.
The teaching or training of patients concerning their own health needs.
Works about lists of drugs or collections of recipes, formulas, and prescriptions for the compounding of medicinal preparations. Formularies differ from PHARMACOPOEIAS in that they are less complete, lacking full descriptions of the drugs, their formulations, analytic composition, chemical properties, etc. In hospitals, formularies list all drugs commonly stocked in the hospital pharmacy.
That segment of commercial enterprise devoted to the design, development, and manufacture of chemical products for use in the diagnosis and treatment of disease, disability, or other dysfunction, or to improve function.
Computer-based systems for input, storage, display, retrieval, and printing of information contained in a patient's medical record.

Diurnal variation in 5-HT1B autoreceptor function in the anterior hypothalamus in vivo: effect of chronic antidepressant drug treatment. (1/521)

1. Intracerebral microdialysis was used to examine the function of the terminal 5-hydroxytryptamine (5-HT) autoreceptor in the anterior hypothalamus of anaesthetized rats at two points in the light phase of the light-dark cycle. 2. Infusion of the 5-HT1A/1B agonist 5-methoxy-3-(1,2,3,6-tetrahydro-4-pyridyl)-1H-indole (RU24969) 0.1, 1.0 and 10 microM through the microdialysis probe led to a concentration-dependent decrease (49, 56 and 65% respectively) in 5-HT output. The effect of RU24969 (1 and 5 microM) was prevented by concurrent infusion of methiothepin (1 and 10 microM) into the anterior hypothalamus via the microdialysis probe. Infusion of methiothepin alone (1.0 and 10 microM) increased (15 and 142% respectively) 5-HT output. 3. Infusion of RU24969 (5 microM) through the probe at mid-light and end-light resulted in a quantitatively greater decrease in 5-HT output at end-light compared with mid-light. 4. Following treatment with either paroxetine hydrochloride (10 mg kg(-1) i.p.) or desipramine hydrochloride (10 mg kg)(-1) i.p.) for 21 days the function of the terminal 5-HT1B autoreceptor was more markedly attenuated at end-light. 5. The data show that, as defined by the response to RU24969, the function of the 5-HT1B receptors that control 5-HT output in the anterior hypothalamus is attenuated following chronic desipramine or paroxetine treatment in a time-of-day-dependent manner.  (+info)

Neuronal uptake affects dynamic characteristics of heart rate response to sympathetic stimulation. (2/521)

Recently, studies in our laboratory involving the use of a Gaussian white noise technique demonstrated that the transfer function from sympathetic stimulation frequency to heart rate (HR) response showed dynamic characteristics of a second-order low-pass filter. However, determinants for the characteristics remain to be established. We examined the effect of an increase in mean sympathetic stimulation frequency and that of a blockade of the neuronal uptake mechanism on the transfer function in anesthetized rabbits. We found that increasing mean sympathetic stimulation frequency from 1 to 4 Hz significantly (P < 0.01) decreased the dynamic gain of the transfer function without affecting other parameters, such as the natural frequency, lag time, or damping coefficient. In contrast, the administration of desipramine (0.3 mg/kg iv), a neuronal uptake blocking agent, significantly (P < 0.01) decreased both the dynamic gain and the natural frequency and prolonged the lag time. These results suggest that the removal rate of norepinephrine at the neuroeffector junction, rather than the amount of available norepinephrine, plays an important role in determining the low-pass filter characteristics of the HR response to sympathetic stimulation.  (+info)

Alpha 1-adrenergic receptor-mediated increase in the mass of phosphatidic acid and 1,2-diacylglycerol in ischemic rat heart. (3/521)

OBJECTIVE: 1,2-Diacylglycerol (1,2-DAG) and phosphatidic acid (PA) are produced by phospholipase C and D activity and play a key role as second messengers in receptor-mediated signal transduction. So far, little is known about alterations of endogenous 1,2-DAG and PA production during myocardial ischemia. METHODS: Rat isolated perfused hearts were subjected to global ischemia, total lipids were extracted, and separated by thin-layer chromatography. The mass of PA and 1,2-DAG were quantified using laserdensitometric analysis of visualized lipids. RESULTS: Compared to normoxic control values (1,2-DAG 713 +/- 45 ng/mg protein, PA 171 +/- 11 ng/mg protein), the myocardial content of 1,2-DAG and PA was unaltered after 10 min of ischemia. Prolonged myocardial ischemia (20 min), however, which was accompanied by marked overflow of endogenous norepinephrine, significantly increased the mass of both second messengers (1,2-DAG 1062 +/- 100 ng/mg protein, PA 340 +/- 29 ng/mg protein). The increase in PA and 1,2-DAG in response to ischemia was abolished by inhibition of ischemia-induced norepinephrine release as well as by alpha1-adrenergic blockade but unaffected by beta-adrenergic blockade. While inhibition of diacylglycerol kinase did not affect ischemia-induced increase in PA and 1,2-DAG, inhibition of phosphatidylinositol-specific phospholipase C activity significantly suppressed ischemia-induced increase in 1,2-DAG but did not affect endogenous production of PA indicating phospholipase C-independent formation of PA and activation of both, phospholipase C and D, in the ischemic heart. CONCLUSIONS: Ischemia elicits an alpha1-adrenergic receptor-mediated increase in the mass of myocardial PA and 1,2-DAG. The increase in endogenous PA is suggested to be due to the activation of myocardial phospholipase D, whereas 1,2-DAG is formed predominantly by activation of phospholipase C in the ischemic heart.  (+info)

Enhancement of the serotonin-mediated acetylcholine release by repeated desmethylimipramine treatment in the hippocampus of freely moving rats. (4/521)

A possible involvement of serotonin-mediated cholinergic activation in the antidepressant effect of desmethylimipramine (DMI) was investigated by determination of the effects of a single or repeated DMI administration on acetylcholine (ACh) release in the hippocampus using an in vivo microdialysis technique and a radioimmunoassay for ACh. Rats were administered DMI (10 mg/kg, i.p.) acutely or repeatedly for 21 days. A single or repeated DMI administration did not cause any significant effects on the basal ACh release compared with the respective controls. Atropine perfusion in the acutely DMI-treated or control rats increased the ACh release to the same degree. In repeatedly DMI-treated rats, serotonin (5-HT) (1 to 10 microM) perfusion enhanced significantly the ACh release. However, 5-HT in acutely DMI-treated rats enhanced significantly the ACh release only at 10 microM. 5-HT did not cause any changes in ACh release in control rats. Hippocampal 5-HT content of acutely DMI-treated rats was significantly higher than that of saline-treated control rats, while no difference was observed between the repeatedly DMI- and saline-treated rats. These findings suggest, for the first time, that DMI induced a facilitation of cholinergic neurotransmission in the rat hippocampus through the activation of 5-HT-receptor function.  (+info)

Electrochemical and electrophysiological characterization of neurotransmitter release from sympathetic nerves supplying rat mesenteric arteries. (5/521)

1. Characteristic features of noradrenaline (NA) and adenosine 5'-triphosphate (ATP) release from postganglionic sympathetic nerves in rat small mesenteric arteries in vitro have been investigated on an impulse-by-impulse basis. NA release was measured using continuous amperometry and ATP release was monitored by intracellular recording of excitatory junction potentials (e.j.ps). 2. Electrical stimuli evoked transient increases in oxidation current. During trains of ten stimuli at 0.5 - 4 Hz there was a depression in the amplitude of oxidation currents evoked following the first stimulus in the train. 3. The neuronal NA uptake inhibitor, desmethylimipramine (1 microM), increased the amplitude of the summed oxidation current evoked by ten stimuli at 1 Hz and slowed the decay of oxidation currents evoked by trains of ten stimuli at 1 and 10 Hz. 4. The alpha2-adrenoceptor antagonist, idazoxan (1 microM), increased the amplitudes of the oxidation currents evoked during trains of ten stimuli at 0.5 - 10 Hz but had no effect on the oxidation currents evoked by the first stimulus in the train. 5. Idazoxan (1 microM) increased the amplitude of all e.j.ps evoked during trains of stimuli at 0.5 and 1 Hz. In addition, the facilitatory effect of idazoxan on e.j.ps was significantly greater than that on oxidation currents. 6. The findings indicate that NA release from sympathetic nerves supplying small mesenteric arteries is regulated by activation of presynaptic alpha2-adrenoceptors and that clearance of released NA in this tissue depends, in part, upon neuronal uptake. The different effects of idazoxan on the oxidation currents and e.j.ps may indicate that the release of NA and ATP is differentially modulated.  (+info)

Comparison of the effects of venlafaxine, desipramine, and paroxetine on noradrenaline- and methoxamine-evoked constriction of the dorsal hand vein. (6/521)

AIMS: To examine whether the antidepressant venlafaxine, a novel serotonin-noradrenaline re-uptake inhibitor (SNRI), can modify alpha-adrenoceptor-mediated venoconstriction in man. The effects of venlafaxine were compared with those of desipramine, a tricyclic antidepressant with noradrenaline uptake inhibiting properties, and paroxetine, a selective serotonin re-uptake inhibitor (SSRI), on noradrenaline-and methoxamine-evoked venoconstriction using the dorsal hand vein compliance technique. METHODS: Fifteen healthy male volunteers participated in five weekly experimental sessions. Each session was associated with a clinically effective dose of an antidepressant or placebo. The following oral dosages were used: venlafaxine 75 mg, venlafaxine 150 mg, desipramine 100 mg, paroxetine 20 mg, or placebo. A double-blind, cross-over, balanced design was used. In each session, dose-response curves to both locally infused noradrenaline acid tartrate (0.1-33.33 ng min-1 ) and methoxamine hydrochloride (0.5-121.5 microg min-1 ) were constructed. Systolic and diastolic blood pressure and pulse rate were measured in the supine and erect positions. Salivation was measured by the dental roll technique. RESULTS: Venlafaxine 150 mg and desipramine 100 mg potentiated the venoconstrictor response to noradrenaline (anova of log ED50s: P<0.01; individual comparisons: venlafaxine 150 mg vs placebo: P<0.005; mean difference, 95% CI: -0. 49 (-0.81, -0.17); desipramine 100 mg vs placebo: P<0.005; mean difference, 95% CI: -0.34 (-0.60, -0.09) without affecting the response to methoxamine. Neither paroxetine nor placebo had any effects on the venoconstrictor responses. Both doses of venlafaxine increased systolic blood pressure (supine and erect) and venlafaxine 150 mg increased diastolic blood pressure (supine) (anova, P<0.05). Desipramine increased heart rate (P<0.05). Desipramine and both doses of venlafaxine reduced salivation (P<0.025). CONCLUSIONS: These results show that, similarly to desipramine 100 mg, venlafaxine 150 mg can potentiate venoconstrictor responses to noradrenaline, consistent with venlafaxine's ability to block noradrenaline uptake in man. The importance of noradrenaline uptake blockade in these observations is confirmed by the lack of effect of the antidepressants on methoxamine-evoked venoconstriction and the failure of paroxetine to modify noradrenaline-evoked venoconstriction.  (+info)

Comparison of the novel antipsychotic ziprasidone with clozapine and olanzapine: inhibition of dorsal raphe cell firing and the role of 5-HT1A receptor activation. (7/521)

Ziprasidone is a novel antipsychotic agent which binds with high affinity to 5-HT1A receptors (Ki = 3.4 nM), in addition to 5-HT1D, 5-HT2, and D2 sites. While it is an antagonist at these latter receptors, ziprasidone behaves as a 5-HT1A agonist in vitro in adenylate cyclase measurements. The goal of the present study was to examine the 5-HT1A properties of ziprasidone in vivo using as a marker of central 5-HT1A activity the inhibition of firing of serotonin-containing neurons in the dorsal raphe nucleus. In anesthetized rats, ziprasidone dose-dependently slowed raphe unit activity (ED50 = 300 micrograms/kg i.v.) as did the atypical antipsychotics clozapine (ED50 = 250 micrograms/kg i.v.) and olanzapine (ED50 = 1000 micrograms/kg i.v.). Pretreatment with the 5-HT1A antagonist WAY-100,635 (10 micrograms/kg i.v.) prevented the ziprasidone-induced inhibition; the same dose of WAY-100,635 had little effect on the inhibition produced by clozapine and olanzapine. Because all three agents also bind to alpha 1 receptors, antagonists of which inhibit serotonin neuronal firing, this aspect of their pharmacology was assessed with desipramine (DMI), a NE re-uptake blocker previously shown to reverse the effects of alpha 1 antagonists on raphe unit activity. DMI (5 mg/kg i.v.) failed to reverse the inhibitory effect of ziprasidone but produced nearly complete reversal of that of clozapine and olanzapine. These profiles suggest a mechanism of action for each agent, 5-HT1A agonism for ziprasidone and alpha 1 antagonism for clozapine and olanzapine. The 5-HT1A agonist activity reported here clearly distinguishes ziprasidone from currently available antipsychotic agents and suggests that this property may play a significant role in its pharmacologic actions.  (+info)

LLC-PK(1) cells stably expressing the human norepinephrine transporter: A functional model of carrier-mediated norepinephrine release in protracted myocardial ischemia. (8/521)

In myocardial ischemia, adrenergic terminals undergo ATP depletion, hypoxia, and intracellular pH reduction, causing the accumulation of axoplasmic norepinephrine (NE) and intracellular Na(+) [via the Na(+)-H(+) exchanger (NHE)]. This forces the reversal of the Na(+)- and Cl(-)-dependent NE transporter (NET), triggering massive carrier-mediated NE release and, thus, arrhythmias. We have now developed a cellular model of carrier-mediated NE release using an LLC-PK(1) cell line stably transfected with human NET cDNA (LLC-NET). LLC-NET cells transported [(3)H]NE and [(3)H]N-methyl-4-phenylpyridinium ([(3)H]MPP(+)) in an inward direction. This uptake was abolished by the NET inhibitors desipramine (100 nM) and mazindol (300 nM) and by extracellular Na(+) removal. Na(+)-gradient reversal induced an efflux of (3)H-substrate from preloaded LLC-NET cells. Desipramine and mazindol blocked this efflux. Because of its greater intracellular stability and higher sensitivity to Na(+)-gradient reversal, [(3)H]MPP(+) proved preferable to [(3)H]NE as an NET substrate; therefore, only [(3)H]MPP(+) was used for subsequent studies. The K(+)/H(+) ionophore nigericin (10 microM) evoked a large efflux of [(3)H]MPP(+). This efflux was potentiated by the Na(+),K(+)-ATPase inhibitor ouabain (100 microM), was sensitive to desipramine, and was blocked by the NHE inhibitor 5-(N-ethyl-N-isopropyl)-amiloride (EIPA; 10 microM). In contrast, EIPA failed to inhibit the [(3)H]MPP(+) efflux elicited by the Na(+) ionophore gramicidin (10 microM). Furthermore, [(3)H]MPP(+) efflux induced by the NHE-stimulant proprionate (25 mM) was negatively modulated by imidazoline receptor activation. Our findings suggest that LLC-NET cells are a sensitive model for studying transductional processes of carrier-mediated NE release associated with myocardial ischemia.  (+info)

Desipramine is a tricyclic antidepressant (TCA) that is primarily used to treat depression. It works by increasing the levels of certain neurotransmitters, such as norepinephrine and serotonin, in the brain. These neurotransmitters are important for maintaining mood, emotion, and behavior.

Desipramine is also sometimes used off-label to treat other conditions, such as anxiety disorders, chronic pain, and attention deficit hyperactivity disorder (ADHD). It is available in oral form and is typically taken one to three times a day.

Like all medications, desipramine can cause side effects, which can include dry mouth, blurred vision, constipation, dizziness, and drowsiness. More serious side effects are rare but can include heart rhythm problems, seizures, and increased suicidal thoughts or behavior in some people, particularly children and adolescents.

It is important to take desipramine exactly as prescribed by a healthcare provider and to report any bothersome or unusual symptoms promptly. Regular follow-up appointments with a healthcare provider are also recommended to monitor the effectiveness and safety of the medication.

Tricyclic antidepressants (TCAs) are a class of medications that were commonly used to treat depression. The name "tricyclic" comes from the chemical structure of these drugs, which contain three rings in their molecular makeup. TCAs were first developed in the 1950s and remained a popular choice for treating depression until the introduction of selective serotonin reuptake inhibitors (SSRIs) in the late 1980s.

TCAs work by increasing the levels of neurotransmitters, such as serotonin and norepinephrine, in the brain. Neurotransmitters are chemical messengers that transmit signals between nerve cells. By increasing the levels of these neurotransmitters, TCAs can help to improve mood and alleviate symptoms of depression.

Some common examples of tricyclic antidepressants include amitriptyline, imipramine, and nortriptyline. While TCAs are effective in treating depression, they can have significant side effects, including dry mouth, blurred vision, constipation, and drowsiness. In addition, TCAs can be dangerous in overdose and may increase the risk of suicide in some individuals. As a result, they are typically used as a last resort when other treatments have failed.

Overall, tricyclic antidepressants are a class of medications that were commonly used to treat depression but have largely been replaced by newer drugs due to their side effects and potential risks.

Adrenergic uptake inhibitors are a class of medications that work by blocking the reuptake of neurotransmitters, such as norepinephrine and dopamine, into the presynaptic neuron. This results in an increase in the amount of neurotransmitter available to bind to postsynaptic receptors, leading to an enhancement of adrenergic transmission.

These medications are used in the treatment of various medical conditions, including depression, attention deficit hyperactivity disorder (ADHD), and narcolepsy. Some examples of adrenergic uptake inhibitors include:

* Tricyclic antidepressants (TCAs): These medications, such as imipramine and amitriptyline, were developed in the 1950s and are used to treat depression, anxiety disorders, and chronic pain.
* Selective serotonin-norepinephrine reuptake inhibitors (SNRIs): These medications, such as venlafaxine and duloxetine, were developed in the 1990s and are used to treat depression, anxiety disorders, and chronic pain.
* Norepinephrine-dopamine reuptake inhibitors (NDRIs): These medications, such as bupropion, are used to treat depression and ADHD.

It's important to note that these medications can have side effects and should be used under the supervision of a healthcare provider.

Imipramine is a tricyclic antidepressant (TCA) medication that is primarily used to treat depression. It works by increasing the levels of certain neurotransmitters, such as serotonin and norepinephrine, in the brain. Imipramine has been found to be effective in treating various types of depression, including major depressive disorder, dysthymia, and depression that is resistant to other treatments.

In addition to its antidepressant effects, imipramine is also used off-label for the treatment of several other conditions, such as anxiety disorders, attention deficit hyperactivity disorder (ADHD), enuresis (bedwetting), and chronic pain.

Imipramine was first synthesized in the 1950s and has been widely used since then. It is available in various forms, including immediate-release tablets, extended-release capsules, and liquid solutions. As with all medications, imipramine can have side effects, which may include dry mouth, blurred vision, constipation, dizziness, and sedation. In rare cases, it can cause more serious side effects, such as cardiac arrhythmias or seizures.

It is important to use imipramine under the close supervision of a healthcare provider, as dosages may need to be adjusted based on individual patient needs and responses to treatment. Additionally, imipramine should not be stopped abruptly, as doing so can lead to withdrawal symptoms or a recurrence of depression.

Antidepressive agents are a class of medications used to treat various forms of depression and anxiety disorders. They act on neurotransmitters, the chemical messengers in the brain, to restore the balance that has been disrupted by mental illness. The most commonly prescribed types of antidepressants include selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), and monoamine oxidase inhibitors (MAOIs). These medications can help alleviate symptoms such as low mood, loss of interest in activities, changes in appetite and sleep patterns, fatigue, difficulty concentrating, and thoughts of death or suicide. It is important to note that antidepressants may take several weeks to reach their full effectiveness and may cause side effects, so it is essential to work closely with a healthcare provider to find the right medication and dosage.

Fluoxetine is a selective serotonin reuptake inhibitor (SSRI) medication that is primarily used to treat major depressive disorder, obsessive-compulsive disorder, bulimia nervosa, panic disorder, and premenstrual dysphoric disorder. It works by increasing the levels of serotonin, a neurotransmitter in the brain that helps maintain mental balance.

Fluoxetine is available under the brand name Prozac and is also available as a generic medication. It comes in various forms, including capsules, tablets, delayed-release capsules, and liquid solution. The typical starting dose for adults with depression is 20 mg per day, but the dosage may be adjusted based on individual patient needs and response to treatment.

Fluoxetine has a relatively long half-life, which means it stays in the body for an extended period of time. This can be beneficial for patients who may have difficulty remembering to take their medication daily, as they may only need to take it once or twice a week. However, it also means that it may take several weeks for the full effects of the medication to become apparent.

As with any medication, fluoxetine can cause side effects, including nausea, dry mouth, sleepiness, insomnia, dizziness, and headache. In some cases, it may also increase the risk of suicidal thoughts or behavior in children, adolescents, and young adults, particularly during the initial stages of treatment. It is important for patients to discuss any concerns about side effects with their healthcare provider.

Clomipramine is a tricyclic antidepressant drug that is primarily used to treat obsessive-compulsive disorder (OCD). It works by increasing the levels of certain neurotransmitters, such as serotonin and norepinephrine, in the brain. These neurotransmitters are involved in regulating mood and behavior.

Clomipramine is also used off-label to treat other conditions, including panic disorder, depression, chronic pain, and sleep disorders. It is available as a tablet or capsule and is typically taken one to three times a day. Common side effects of clomipramine include dry mouth, constipation, blurred vision, dizziness, and drowsiness.

As with all medications, clomipramine should be used under the close supervision of a healthcare provider, who can monitor its effectiveness and potential side effects. It is important to follow the dosage instructions carefully and to report any unusual symptoms or concerns to the healthcare provider promptly.

Norepinephrine plasma membrane transport proteins, also known as norepinephrine transporters (NET), are membrane-bound proteins that play a crucial role in the regulation of neurotransmission. They are responsible for the reuptake of norepinephrine from the synaptic cleft back into the presynaptic neuron, thereby terminating the signal transmission and preventing excessive stimulation of postsynaptic receptors.

The norepinephrine transporter is a member of the sodium-dependent neurotransmitter transporter family and functions as an antiporter, exchanging one intracellular sodium ion for two extracellular sodium ions along with the transport of norepinephrine. This sodium gradient provides the energy required for the active transport process.

Dysregulation of norepinephrine plasma membrane transport proteins has been implicated in various neurological and psychiatric disorders, such as attention deficit hyperactivity disorder (ADHD), depression, and post-traumatic stress disorder (PTSD). Therefore, understanding the function and regulation of these transporters is essential for developing novel therapeutic strategies to treat these conditions.

Protriptyline is a tricyclic antidepressant (TCA) medication. It is primarily used to treat symptoms of depression, but it can also be used for other conditions such as anxiety disorders or to help manage chronic pain. Protriptyline works by increasing the levels of certain neurotransmitters in the brain, such as norepinephrine and serotonin, which can help to improve mood and reduce symptoms of depression.

Protriptyline has a sedating effect, so it may also be used to treat insomnia or agitation associated with depression. It is available in immediate-release tablet form and is typically taken two to four times per day. As with all medications, protriptyline can have side effects, including dry mouth, blurred vision, constipation, and dizziness. It may also cause cardiac arrhythmias and should be used with caution in patients with a history of heart disease.

It's important to note that the use of Protriptyline and other tricyclic antidepressants has declined over the years due to the development of newer classes of antidepressants, such as selective serotonin reuptake inhibitors (SSRIs), which have fewer side effects and are safer in overdose. However, protriptyline may still be prescribed in certain cases where other treatments have not been effective.

Norepinephrine, also known as noradrenaline, is a neurotransmitter and a hormone that is primarily produced in the adrenal glands and is released into the bloodstream in response to stress or physical activity. It plays a crucial role in the "fight-or-flight" response by preparing the body for action through increasing heart rate, blood pressure, respiratory rate, and glucose availability.

As a neurotransmitter, norepinephrine is involved in regulating various functions of the nervous system, including attention, perception, motivation, and arousal. It also plays a role in modulating pain perception and responding to stressful or emotional situations.

In medical settings, norepinephrine is used as a vasopressor medication to treat hypotension (low blood pressure) that can occur during septic shock, anesthesia, or other critical illnesses. It works by constricting blood vessels and increasing heart rate, which helps to improve blood pressure and perfusion of vital organs.

Amitriptyline is a type of medication known as a tricyclic antidepressant (TCA). It is primarily used to treat depression, but it also has other therapeutic uses such as managing chronic pain, migraine prevention, and treating anxiety disorders. Amitriptyline works by increasing the levels of certain neurotransmitters (chemical messengers) in the brain, such as serotonin and norepinephrine, which help to regulate mood and alleviate pain.

The medication is available in various forms, including tablets and liquid solutions, and it is typically taken orally. The dosage of amitriptyline may vary depending on the individual's age, medical condition, and response to treatment. It is essential to follow the prescribing physician's instructions carefully when taking this medication.

Common side effects of amitriptyline include drowsiness, dry mouth, blurred vision, constipation, and weight gain. In some cases, it may cause more severe side effects such as orthostatic hypotension (low blood pressure upon standing), cardiac arrhythmias, and seizures. It is crucial to inform the healthcare provider of any pre-existing medical conditions or current medications before starting amitriptyline therapy, as these factors can influence its safety and efficacy.

Amitriptyline has a well-established history in clinical practice, but it may not be suitable for everyone due to its potential side effects and drug interactions. Therefore, it is essential to consult with a healthcare professional before using this medication.

Maprotiline is a tetracyclic antidepressant (TCA) medication that is primarily used to treat major depressive disorder. It works by increasing the levels of neurotransmitters, such as norepinephrine and serotonin, in the brain, which can help to improve mood and alleviate symptoms of depression.

Maprotiline has a unique chemical structure that distinguishes it from other antidepressants, including selective serotonin reuptake inhibitors (SSRIs) and tricyclic antidepressants (TCAs). It is considered to be a second-line treatment option for depression, typically reserved for use when other antidepressants have not been effective.

Like other TCAs, maprotiline can cause a range of side effects, including dry mouth, blurred vision, constipation, and dizziness. It may also cause more serious side effects, such as seizures, irregular heartbeat, and changes in blood pressure. As a result, it is important to use maprotiline under the close supervision of a healthcare provider.

Maprotiline is available in tablet form and is typically taken two to four times per day, with or without food. The dosage may be gradually increased over time to achieve the desired therapeutic effect. It may take several weeks of treatment before the full benefits of maprotiline are felt.

Fluvoxamine is a type of antidepressant known as a selective serotonin reuptake inhibitor (SSRI). It works by increasing the levels of serotonin, a neurotransmitter in the brain that helps maintain mental balance. Fluvoxamine is primarily used to treat obsessive-compulsive disorder (OCD) and may also be prescribed for other conditions such as depression, panic disorder, or social anxiety disorder.

The medical definition of Fluvoxamine can be stated as:

Fluvoxamine maleate, a selective serotonin reuptake inhibitor (SSRI), is a psychotropic medication used primarily in the treatment of obsessive-compulsive disorder (OCD). It functions by increasing the availability of serotonin in the synaptic cleft, which subsequently modulates neurotransmission and helps restore emotional balance. Fluvoxamine may also be employed off-label for managing other conditions, such as depression, panic disorder, or social anxiety disorder, subject to clinical judgment and patient needs.

Alpha-2 adrenergic receptors are a type of G protein-coupled receptor that binds catecholamines, such as norepinephrine and epinephrine. These receptors are widely distributed in the central and peripheral nervous system, as well as in various organs and tissues throughout the body.

Activation of alpha-2 adrenergic receptors leads to a variety of physiological responses, including inhibition of neurotransmitter release, vasoconstriction, and reduced heart rate. These receptors play important roles in regulating blood pressure, pain perception, and various cognitive and emotional processes.

There are several subtypes of alpha-2 adrenergic receptors, including alpha-2A, alpha-2B, and alpha-2C, which may have distinct physiological functions and be targeted by different drugs. For example, certain medications used to treat hypertension or opioid withdrawal target alpha-2 adrenergic receptors to produce their therapeutic effects.

Mianserin is a tetracyclic antidepressant (TCA) that is primarily used to treat major depressive disorders. It functions by inhibiting the reuptake of neurotransmitters such as serotonin and noradrenaline, thereby increasing their availability in the brain and helping to alleviate symptoms of depression.

Mianserin also has additional properties, including antihistamine and anti-cholinergic effects, which can help reduce some side effects commonly associated with other antidepressants, such as insomnia and agitation. However, these same properties can also lead to side effects such as drowsiness, dry mouth, and orthostatic hypotension (a drop in blood pressure upon standing).

It's important to note that mianserin is not commonly prescribed due to its narrow therapeutic index and the risk of serious side effects, including agranulocytosis (a severe decrease in white blood cells), which can increase the risk of infection. As with any medication, it should only be taken under the close supervision of a healthcare provider.

Dibenzazepines are a class of chemical compounds that contain a dibenzazepine structure, which is a fusion of a benzene ring with a diazepine ring. Dibenzazepines have a wide range of pharmacological activities and are used in the treatment of various medical conditions.

Some of the medically relevant dibenzazepines include:

1. Antipsychotics: Some antipsychotic drugs, such as clozapine and olanzapine, have a dibenzazepine structure. These drugs are used to treat schizophrenia and other psychotic disorders.
2. Antidepressants: Mianserin and mirtazapine are dibenzazepine antidepressants that work by blocking the uptake of serotonin and noradrenaline in the brain. They are used to treat depression, anxiety, and insomnia.
3. Anticonvulsants: Some anticonvulsant drugs, such as levetiracetam and brivaracetam, have a dibenzazepine structure. These drugs are used to treat epilepsy and other seizure disorders.
4. Anxiolytics: Prazepam is a benzodiazepine derivative with a dibenzazepine structure that is used to treat anxiety disorders.
5. Analgesics: Tramadol is a centrally acting analgesic with a dibenzazepine structure that is used to treat moderate to severe pain.

It's important to note that while these drugs have a dibenzazepine structure, they may also contain other functional groups and have different mechanisms of action. Therefore, it's essential to consider the specific pharmacological properties of each drug when prescribing or administering them.

Nortriptyline is a tricyclic antidepressant (TCA) that is primarily used in the treatment of depression. It works by increasing the levels of certain neurotransmitters, such as serotonin and norepinephrine, in the brain. These neurotransmitters are involved in regulating mood, and increasing their levels can help to alleviate symptoms of depression.

Nortriptyline is available in oral form and is typically taken two or three times a day. It may take several weeks of treatment before the full benefits of the medication are felt. Common side effects of nortriptyline include dry mouth, blurred vision, constipation, and dizziness. In rare cases, it can cause more serious side effects such as heart rhythm problems, seizures, or increased suicidal thoughts or behavior.

Nortriptyline is generally considered to be safe and effective for the treatment of depression, but it should only be used under the close supervision of a healthcare provider due to its potential for serious side effects. It may also interact with other medications, so it is important to inform your doctor of all medications you are taking before starting nortriptyline.

1-Naphthylamine is a crystalline solid with the chemical formula C10H9N. It is an aromatic amine, which means it contains an amino group (-NH2) attached to an aromatic hydrocarbon ring. Specifically, 1-Naphthylamine is derived from naphthalene, a polycyclic aromatic hydrocarbon consisting of two benzene rings fused together.

1-Naphthylamine is a primary amine, which means the amino group is attached directly to the aromatic ring. It is a pale yellow to white crystalline powder with a melting point of 52°C (126°F) and boiling point of 280°C (536°F) at 760 mmHg.

Historically, 1-Naphthylamine was used in the manufacture of dyes and as an intermediate in the production of other chemicals. However, it is now known to be a potent human carcinogen, causing bladder cancer and other types of cancer. Therefore, its use in industrial applications has been largely discontinued.

Nomifensine is a medication that was previously used in the treatment of depression, but it is no longer available in many countries due to safety concerns. It is a non-tricyclic antidepressant that works by inhibiting the reuptake of dopamine and noradrenaline, which helps to increase the levels of these neurotransmitters in the brain and improve mood.

The medical definition of Nomifensine is:

"Nomifensine is a non-tricyclic antidepressant that is a potent inhibitor of dopamine and noradrenaline reuptake, with minimal effects on serotonin reuptake. It was used in the treatment of depression but has been withdrawn from the market due to safety concerns."

It's important to note that Nomifensine should only be taken under the supervision of a medical professional, and it is not available in many countries due to its potential for causing serious side effects such as liver toxicity and the risk of developing a rare but potentially fatal condition called hemolytic anemia.

Sparteine is not typically referred to as a "medical definition" in the context of modern medicine. However, it is a chemical compound with some historical use in medicine and a well-defined chemical structure.

Here's a chemical definition of sparteine:

Sparteine is an alkaloid derived from plants of the genus *Colutea* and *Genista*, but most notably from *Crotalaria sagittalis* (rattlebox) and *Echium plantagineum* (viper's bugloss). Its chemical formula is C15H24N2, and it has a molecular weight of 228.36 g/mol.

Sparteine is a stereoisomer of lupanine and is structurally related to other natural alkaloids such as nicotine and coniine. It is a chiral compound with two stereocenters, existing as four different stereoisomers: (−)-sparteine, (+)-sparteine, (−)-pseudosparteine, and (+)-pseudosparteine.

Historically, sparteine has been used in medicine as a cardiotonic, uterine stimulant, and antispasmodic. However, due to its narrow therapeutic index and the availability of safer alternatives, it is no longer in common clinical use today.

I'm sorry for any confusion, but "swimming" is not typically considered a medical term. It refers to the act of moving through water using your arms and legs in a rhythmic pattern, often as a form of exercise, recreation, or competition. However, if you're referring to a medical condition related to swimming, such as "swimmer's ear" (otitis externa), I would be happy to provide a definition for that.

Swimmer's ear is a type of outer ear infection caused by water remaining in the ear after swimming or bathing, creating a moist environment that can lead to bacterial growth. It can also be caused by scratching or damaging the lining of the ear canal through the use of cotton swabs or other objects. Symptoms may include itching, redness, pain, and sometimes discharge from the ear. If left untreated, swimmer's ear can lead to more serious complications, such as hearing loss or damage to the inner ear.

Tyramine is not a medical condition but a naturally occurring compound called a biogenic amine, which is formed from the amino acid tyrosine during the fermentation or decay of certain foods. Medically, tyramine is significant because it can interact with certain medications, particularly monoamine oxidase inhibitors (MAOIs), used to treat depression and other conditions.

The interaction between tyramine and MAOIs can lead to a hypertensive crisis, a rapid and severe increase in blood pressure, which can be life-threatening if not treated promptly. Therefore, individuals taking MAOIs are often advised to follow a low-tyramine diet, avoiding foods high in tyramine, such as aged cheeses, cured meats, fermented foods, and some types of beer and wine.

5,7-Dihydroxytryptamine is a chemical compound that is a derivative of the neurotransmitter serotonin. It is formed by the hydroxylation of serotonin at the 5 and 7 positions of its indole ring. This compound is not typically found in significant concentrations in the body, but it can be synthesized and used for research purposes.

In the laboratory, 5,7-Dihydroxytryptamine has been used as a tool to study the role of serotonin in various physiological processes. For example, researchers have used this compound to selectively destroy serotonergic neurons in animal models, allowing them to investigate the functions of these neurons and their contributions to behavior and brain function.

It is important to note that 5,7-Dihydroxytryptamine is not a medication or therapeutic agent, and it should only be used in research settings under the guidance of trained professionals.

Mescaline is a naturally occurring psychoactive alkaloid that is found in several species of cacti, including the peyote (Lophophora williamsii), San Pedro (Echinopsis pachanoi), and Peruvian torch (Echinopsis peruviana) cacti. It is known for its ability to produce profound changes in consciousness, mood, and perception when ingested.

In a medical context, mescaline is classified as a hallucinogen or psychedelic drug. It works by binding to serotonin receptors in the brain, which leads to altered states of consciousness, including visual hallucinations, distorted perceptions of time and space, and altered emotional states.

It's important to note that while mescaline has been used for centuries in religious and spiritual practices among indigenous communities, its use is not without risks. High doses can lead to unpleasant or even dangerous psychological effects, such as anxiety, panic, and psychosis. Additionally, the legal status of mescaline varies by country and region, so it's important to be aware of local laws and regulations before using it.

Zimeldine is not commonly used in current medical practice due to its association with serious side effects. However, historically, it was a medication used as an antidepressant. It belongs to the class of drugs called selective serotonin reuptake inhibitors (SSRIs), which work by increasing the levels of the neurotransmitter serotonin in the brain.

Zimeldine was first synthesized in 1972 and approved for medical use in Sweden in 1982. However, it was withdrawn from the market in 1983 due to its association with a rare but serious side effect called Guillain-Barré syndrome, which is a neurological disorder that can cause muscle weakness and paralysis.

Although Zimeldine is no longer used in medical practice, it played an important role in the development of SSRIs as a class of antidepressants, which have since become widely used due to their effectiveness and relatively favorable side effect profile compared to earlier classes of antidepressants.

Clonidine is an medication that belongs to a class of drugs called centrally acting alpha-agonist hypotensives. It works by stimulating certain receptors in the brain and lowering the heart rate, which results in decreased blood pressure. Clonidine is commonly used to treat hypertension (high blood pressure), but it can also be used for other purposes such as managing withdrawal symptoms from opioids or alcohol, treating attention deficit hyperactivity disorder (ADHD), and preventing migraines. It can be taken orally in the form of tablets or transdermally through a patch applied to the skin. As with any medication, clonidine should be used under the guidance and supervision of a healthcare provider.

Paroxetine is a selective serotonin reuptake inhibitor (SSRI) medication that is primarily used to treat major depressive disorders, obsessive-compulsive disorder, panic disorder, social anxiety disorder, generalized anxiety disorder, and post-traumatic stress disorder. It works by increasing the levels of serotonin, a neurotransmitter in the brain that helps maintain mental balance, leading to an improvement in mood and other symptoms associated with these conditions.

Paroxetine is available under various brand names, such as Paxil and Seroxat, and it comes in different forms, including tablets, capsules, and liquid solutions. The medication is typically taken once daily, although the dosage may vary depending on the individual's needs and the specific condition being treated.

As with any medication, paroxetine can have side effects, such as nausea, dizziness, dry mouth, and sleep disturbances. In some cases, it may also cause more serious side effects, including increased risk of suicidal thoughts or behaviors in children, adolescents, and young adults, as well as an increased risk of bleeding and hyponatremia (low sodium levels).

It is important to consult with a healthcare provider before starting paroxetine or any other medication, and to follow their instructions carefully regarding dosage, timing, and potential interactions with other drugs or medical conditions.

Serotonin uptake inhibitors (also known as Selective Serotonin Reuptake Inhibitors or SSRIs) are a class of medications primarily used to treat depression and anxiety disorders. They work by increasing the levels of serotonin, a neurotransmitter in the brain that helps regulate mood, appetite, and sleep, among other functions.

SSRIs block the reuptake of serotonin into the presynaptic neuron, allowing more serotonin to be available in the synapse (the space between two neurons) for binding to postsynaptic receptors. This results in increased serotonergic neurotransmission and improved mood regulation.

Examples of SSRIs include fluoxetine (Prozac), sertraline (Zoloft), paroxetine (Paxil), citalopram (Celexa), and escitalopram (Lexapro). These medications are generally well-tolerated, with side effects that may include nausea, headache, insomnia, sexual dysfunction, and increased anxiety or agitation. However, they can have serious interactions with other medications, so it is important to inform your healthcare provider of all medications you are taking before starting an SSRI.

Metaraminol is a synthetic vasoconstrictor and sympathomimetic agent, which is primarily used in clinical medicine to raise blood pressure in hypotensive states. It is a direct-acting alpha-adrenergic agonist, with some mild beta-adrenergic activity as well.

Metaraminol works by stimulating the alpha-adrenergic receptors in the smooth muscle of blood vessels, causing them to contract and narrow, leading to an increase in peripheral vascular resistance and systolic blood pressure. It also has a positive inotropic effect on the heart, increasing its contractility and stroke volume.

The drug is administered intravenously, and its effects are usually rapid in onset but short-lived, typically lasting for 5 to 10 minutes. Common side effects of metaraminol include hypertension, reflex bradycardia, arrhythmias, headache, anxiety, and tremors. It should be used with caution in patients with ischemic heart disease, hypertension, and other cardiovascular conditions.

A drug interaction is the effect of combining two or more drugs, or a drug and another substance (such as food or alcohol), which can alter the effectiveness or side effects of one or both of the substances. These interactions can be categorized as follows:

1. Pharmacodynamic interactions: These occur when two or more drugs act on the same target organ or receptor, leading to an additive, synergistic, or antagonistic effect. For example, taking a sedative and an antihistamine together can result in increased drowsiness due to their combined depressant effects on the central nervous system.
2. Pharmacokinetic interactions: These occur when one drug affects the absorption, distribution, metabolism, or excretion of another drug. For example, taking certain antibiotics with grapefruit juice can increase the concentration of the antibiotic in the bloodstream, leading to potential toxicity.
3. Food-drug interactions: Some drugs may interact with specific foods, affecting their absorption, metabolism, or excretion. An example is the interaction between warfarin (a blood thinner) and green leafy vegetables, which can increase the risk of bleeding due to enhanced vitamin K absorption from the vegetables.
4. Drug-herb interactions: Some herbal supplements may interact with medications, leading to altered drug levels or increased side effects. For instance, St. John's Wort can decrease the effectiveness of certain antidepressants and oral contraceptives by inducing their metabolism.
5. Drug-alcohol interactions: Alcohol can interact with various medications, causing additive sedative effects, impaired judgment, or increased risk of liver damage. For example, combining alcohol with benzodiazepines or opioids can lead to dangerous levels of sedation and respiratory depression.

It is essential for healthcare providers and patients to be aware of potential drug interactions to minimize adverse effects and optimize treatment outcomes.

Normetanephrine is defined as a major metabolite of epinephrine (adrenaline), which is formed by the action of catechol-O-methyltransferase (COMT) on metanephrine. It is primarily produced in the adrenal gland and is also found in the sympathetic nervous system. Normetanephrine is often measured in clinical testing to help diagnose pheochromocytoma, a rare tumor of the adrenal glands that can cause high blood pressure and other symptoms due to excessive production of catecholamines. Increased levels of normetanephrine in the urine or plasma may indicate the presence of a pheochromocytoma or other conditions associated with increased catecholamine release.

Reserpine is an alkaloid derived from the Rauwolfia serpentina plant, which has been used in traditional medicine for its sedative and hypotensive effects. In modern medicine, reserpine is primarily used to treat hypertension (high blood pressure) due to its ability to lower both systolic and diastolic blood pressure.

Reserpine works by depleting catecholamines, including norepinephrine, epinephrine, and dopamine, from nerve terminals in the sympathetic nervous system. This leads to a decrease in peripheral vascular resistance and heart rate, ultimately resulting in reduced blood pressure.

Reserpine is available in various forms, such as tablets or capsules, and is typically administered orally. Common side effects include nasal congestion, dizziness, sedation, and gastrointestinal disturbances like diarrhea and nausea. Long-term use of reserpine may also lead to depression in some individuals. Due to its potential for causing depression, other antihypertensive medications are often preferred over reserpine when possible.

Second-generation antidepressants (SGAs) are a class of medications used primarily for the treatment of depression, although they are also used for other psychiatric and medical conditions. They are called "second-generation" because they were developed after the first generation of antidepressants, which include tricyclic antidepressants (TCAs) and monoamine oxidase inhibitors (MAOIs).

SGAs are also known as atypical antidepressants or novel antidepressants. They work by affecting the levels of neurotransmitters in the brain, such as serotonin, norepinephrine, and dopamine. However, they have a different chemical structure and mechanism of action than first-generation antidepressants.

Some examples of second-generation antidepressants include:

* Selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine (Prozac), sertraline (Zoloft), and citalopram (Celexa)
* Serotonin-norepinephrine reuptake inhibitors (SNRIs) such as venlafaxine (Effexor) and duloxetine (Cymbalta)
* Norepinephrine and dopamine reuptake inhibitors (NDRIs) such as bupropion (Wellbutrin)
* Atypical antidepressants such as mirtazapine (Remeron), trazodone, and vortioxetine (Brintellix)

SGAs are generally considered to have a more favorable side effect profile than first-generation antidepressants. They are less likely to cause anticholinergic effects such as dry mouth, constipation, and blurred vision, and they are less likely to cause cardiac conduction abnormalities or orthostatic hypotension. However, SGAs may still cause side effects such as nausea, insomnia, sexual dysfunction, and weight gain.

It's important to note that the choice of antidepressant medication should be individualized based on the patient's specific symptoms, medical history, and other factors. It may take some trial and error to find the most effective and well-tolerated medication for a given patient.

Pargyline is an antihypertensive drug and a irreversible monoamine oxidase inhibitor (MAOI) of type B. It works by blocking the breakdown of certain chemicals in the brain, such as neurotransmitters, which can help improve mood and behavior in people with depression.

Pargyline is not commonly used as a first-line treatment for depression due to its potential for serious side effects, including interactions with certain foods and medications that can lead to dangerously high blood pressure. It is also associated with a risk of serotonin syndrome when taken with selective serotonin reuptake inhibitors (SSRIs) or other drugs that increase serotonin levels in the brain.

Pargyline is available only through a prescription and should be used under the close supervision of a healthcare provider.

Cyclohexanols are a class of organic compounds that contain a cyclohexane ring (a six-carbon saturated ring) with a hydroxyl group (-OH) attached to it. The hydroxyl group makes these compounds alcohols, and the cyclohexane ring provides a unique structure that can adopt different conformations.

The presence of the hydroxyl group in cyclohexanols allows them to act as solvents, intermediates in chemical synthesis, and starting materials for the production of other chemicals. They are used in various industries, including pharmaceuticals, agrochemicals, and polymers.

Cyclohexanols can exist in different forms, such as cis- and trans-isomers, depending on the orientation of the hydroxyl group relative to the cyclohexane ring. The physical and chemical properties of these isomers can differ significantly due to their distinct structures and conformations.

Examples of cyclohexanols include cyclohexanol itself (C6H11OH), as well as its derivatives, such as methylcyclohexanol (C7H13OH) and phenylcyclohexanol (C12H15OH).

Galactosylgalactosylglucosylceramidase is a type of enzyme that is involved in the breakdown and recycling of complex lipids called glycosphingolipids in the body. More specifically, it helps to break down a particular type of glycosphingolipid known as globotriaosylceramide (Gb3 or CD77) into simpler components.

This enzyme is critical for maintaining the health and function of various tissues in the body, including the nervous system. Deficiencies in galactosylgalactosylglucosylceramidase have been linked to a number of serious genetic disorders, such as Tay-Sachs disease and Sandhoff disease, which are characterized by the accumulation of Gb3 and other glycosphingolipids in various tissues, leading to progressive neurological deterioration and other symptoms.

Serotonin, also known as 5-hydroxytryptamine (5-HT), is a monoamine neurotransmitter that is found primarily in the gastrointestinal (GI) tract, blood platelets, and the central nervous system (CNS) of humans and other animals. It is produced by the conversion of the amino acid tryptophan to 5-hydroxytryptophan (5-HTP), and then to serotonin.

In the CNS, serotonin plays a role in regulating mood, appetite, sleep, memory, learning, and behavior, among other functions. It also acts as a vasoconstrictor, helping to regulate blood flow and blood pressure. In the GI tract, it is involved in peristalsis, the contraction and relaxation of muscles that moves food through the digestive system.

Serotonin is synthesized and stored in serotonergic neurons, which are nerve cells that use serotonin as their primary neurotransmitter. These neurons are found throughout the brain and spinal cord, and they communicate with other neurons by releasing serotonin into the synapse, the small gap between two neurons.

Abnormal levels of serotonin have been linked to a variety of disorders, including depression, anxiety, schizophrenia, and migraines. Medications that affect serotonin levels, such as selective serotonin reuptake inhibitors (SSRIs), are commonly used to treat these conditions.

Sertraline is a medication that belongs to a class of drugs called selective serotonin reuptake inhibitors (SSRIs). It is primarily used to treat depression, obsessive-compulsive disorder, panic disorder, post-traumatic stress disorder, social anxiety disorder, and in some cases, premenstrual dysphoric disorder.

Sertraline works by increasing the levels of serotonin, a neurotransmitter in the brain that helps maintain mental balance, in the synaptic cleft (the space between two nerve cells where neurotransmitters are released and received). By inhibiting the reuptake of serotonin, sertraline enhances the signal strength and duration of action of this neurotransmitter, which can help alleviate symptoms associated with various mental health conditions.

It is important to note that sertraline should only be taken under the supervision of a healthcare professional, as it may have side effects and potential interactions with other medications. Always consult a medical provider for personalized advice regarding medication use.

Phenelzine is a type of medication known as a non-selective, irreversible monoamine oxidase inhibitor (MAOI). It works by blocking the action of an enzyme called monoamine oxidase, which breaks down certain chemicals in the brain such as neurotransmitters (e.g., serotonin, norepinephrine, dopamine). This leads to an increase in the levels of these neurotransmitters in the brain, which can help improve mood and alleviate symptoms of depression.

Phenelzine is primarily used off-label for the treatment of depression that has not responded to other antidepressant medications. It is also used for the treatment of anxiety disorders, including panic disorder and social anxiety disorder.

It's important to note that MAOIs like phenelzine have several dietary restrictions and potential serious drug interactions due to their mechanism of action. Therefore, they are typically considered a last resort when other antidepressants have failed.

Neurotransmitter uptake inhibitors are a class of drugs that work by blocking the reuptake of neurotransmitters, such as serotonin, norepinephrine, and dopamine, into the presynaptic neuron after they have been released into the synapse. This results in an increased concentration of these neurotransmitters in the synapse, which can enhance their signal transduction and lead to therapeutic effects.

These drugs are commonly used in the treatment of various psychiatric disorders, such as depression, anxiety, and attention deficit hyperactivity disorder (ADHD). They include selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), and norepinephrine reuptake inhibitors (NRIs).

It's important to note that while neurotransmitter uptake inhibitors can be effective in treating certain conditions, they may also have potential side effects and risks. Therefore, it is essential to use them under the guidance and supervision of a healthcare professional.

Methoxamine is a synthetic, selective α1-adrenergic receptor agonist used in scientific research and for therapeutic purposes. It has the ability to stimulate the α1 adrenergic receptors, leading to vasoconstriction (constriction of blood vessels), increased blood pressure, and reduced blood flow to the skin and extremities.

In a medical context, methoxamine is primarily used as an experimental drug or in research settings due to its specific pharmacological properties. It may be employed to investigate the role of α1-adrenergic receptors in various physiological processes or to temporarily counteract the hypotensive (low blood pressure) effects of certain medications, such as vasodilators or anesthetics.

It is important to note that methoxamine is not commonly used in routine clinical practice due to its strong vasoconstrictive properties and potential adverse effects on organ function if misused or improperly dosed.

Alpha-Methyltyrosine (α-MT) is a synthetic amino acid that acts as an inhibitor of the enzyme tyrosine hydroxylase. This enzyme is a rate-limiting step in the biosynthesis of catecholamines, including neurotransmitters such as dopamine and norepinephrine. By inhibiting tyrosine hydroxylase, α-MT reduces the synthesis of these catecholamines, which can lead to various effects on the nervous system.

In medical contexts, α-MT has been used in research settings to study the functions of catecholamines and their role in various physiological processes. It has also been investigated as a potential treatment for certain conditions, such as hypertension and anxiety disorders, although its clinical use is not widespread due to its side effects and limited efficacy.

It's important to note that α-MT should only be used under the supervision of a medical professional, as it can have significant effects on the nervous system and may interact with other medications or health conditions.

Adrenergic neurons are specialized type of nerve cells that release and utilize catecholamines, particularly norepinephrine (noradrenaline) and to a lesser extent, epinephrine (adrenaline), as their primary neurotransmitters. These neurotransmitters play crucial roles in the body's sympathetic nervous system, which is responsible for the "fight or flight" response during stressful situations.

Adrenergic neurons are primarily located in the central nervous system (CNS) and the peripheral nervous system (PNS). In the CNS, they are found mainly in brainstem nuclei, such as the locus coeruleus, which is the primary source of norepinephrine. In the PNS, adrenergic neurons are part of the sympathetic ganglia and innervate various target organs, including the heart, blood vessels, lungs, glands, and other smooth muscles.

The activation of adrenergic receptors by norepinephrine or epinephrine leads to a range of physiological responses, such as increased heart rate, contractility, and blood pressure; bronchodilation in the lungs; and modulation of pain perception, attention, and arousal in the CNS. Dysfunction of adrenergic neurons has been implicated in several neurological and psychiatric disorders, including depression, anxiety, post-traumatic stress disorder (PTSD), and neurodegenerative diseases like Parkinson's disease.

Cytochrome P-450 CYP2D6 is a specific isoenzyme belonging to the Cytochrome P-450 (CYP) family of enzymes, which are primarily located in the liver and play a crucial role in the metabolism of various drugs and xenobiotics. The term "P-450" refers to the absorption spectrum of these enzymes when they are combined with carbon monoxide, exhibiting a peak absorbance at 450 nanometers.

CYP2D6 is involved in the metabolism of approximately 20-25% of clinically prescribed drugs, including many antidepressants, neuroleptics, beta-blockers, opioids, and antiarrhythmics. This enzyme can demonstrate genetic polymorphisms, leading to variations in drug metabolism rates among individuals. These genetic differences can result in four distinct phenotypes: poor metabolizers (PM), intermediate metabolizers (IM), extensive metabolizers (EM), and ultra-rapid metabolizers (UM).

Poor metabolizers have decreased or absent CYP2D6 enzyme activity due to genetic mutations, leading to an accumulation of drugs in the body and increased susceptibility to adverse drug reactions. In contrast, ultra-rapid metabolizers possess multiple copies of the functional CYP2D6 gene, resulting in enhanced enzymatic activity and rapid drug clearance. This can lead to therapeutic failure due to insufficient drug exposure at the target site.

Understanding the genetic variations in CYP2D6 is essential for personalized medicine, as it allows healthcare providers to tailor drug therapy based on an individual's metabolic capacity and minimize the risk of adverse reactions or treatment failures.

Adrenergic agents are a class of drugs that bind to and activate adrenergic receptors, which are cell surface receptors found in the nervous system and other tissues. These receptors are activated by neurotransmitters such as norepinephrine and epinephrine (also known as adrenaline), which are released by the sympathetic nervous system in response to stress or excitement.

Adrenergic agents can be classified based on their mechanism of action and the specific receptors they bind to. There are two main types of adrenergic receptors: alpha and beta receptors, each with several subtypes. Some adrenergic agents bind to both alpha and beta receptors, while others are selective for one or the other.

Adrenergic agents have a wide range of therapeutic uses, including the treatment of asthma, cardiovascular diseases, glaucoma, and neurological disorders. They can also be used as diagnostic tools to test the function of the sympathetic nervous system. Some examples of adrenergic agents include:

* Alpha-agonists: These drugs bind to alpha receptors and cause vasoconstriction (narrowing of blood vessels), which can be useful in the treatment of hypotension (low blood pressure) or nasal congestion. Examples include phenylephrine and oxymetazoline.
* Alpha-antagonists: These drugs block the action of alpha receptors, leading to vasodilation (widening of blood vessels) and a decrease in blood pressure. Examples include prazosin and doxazosin.
* Beta-agonists: These drugs bind to beta receptors and cause bronchodilation (opening of the airways), increased heart rate, and increased force of heart contractions. They are used in the treatment of asthma, chronic obstructive pulmonary disease (COPD), and other respiratory disorders. Examples include albuterol and salmeterol.
* Beta-antagonists: These drugs block the action of beta receptors, leading to a decrease in heart rate, blood pressure, and bronchodilation. They are used in the treatment of hypertension, angina (chest pain), and heart failure. Examples include metoprolol and atenolol.
* Nonselective alpha- and beta-antagonists: These drugs block both alpha and beta receptors and are used in the treatment of hypertension, angina, and heart failure. Examples include labetalol and carvedilol.

Biogenic monoamines are a type of neurotransmitter, which are chemical messengers that transmit signals in the brain and other parts of the nervous system. They are called "biogenic" because they are derived from biological substances, and "monoamines" because they contain one amine group (-NH2) and are derived from the aromatic amino acids: tryptophan, tyrosine, and phenylalanine.

Examples of biogenic monoamines include:

1. Serotonin (5-hydroxytryptamine or 5-HT): synthesized from the amino acid tryptophan and plays a crucial role in regulating mood, appetite, sleep, memory, and learning.
2. Dopamine: formed from tyrosine and is involved in reward, motivation, motor control, and reinforcement of behavior.
3. Norepinephrine (noradrenaline): also derived from tyrosine and functions as a neurotransmitter and hormone that modulates attention, arousal, and stress responses.
4. Epinephrine (adrenaline): synthesized from norepinephrine and serves as a crucial hormone and neurotransmitter in the body's fight-or-flight response to stress or danger.
5. Histamine: produced from the amino acid histidine, it acts as a neurotransmitter and mediates allergic reactions, immune responses, and regulates wakefulness and appetite.

Imbalances in biogenic monoamines have been linked to various neurological and psychiatric disorders, such as depression, anxiety, Parkinson's disease, and schizophrenia. Therefore, medications that target these neurotransmitters, like selective serotonin reuptake inhibitors (SSRIs) for depression or levodopa for Parkinson's disease, are often used in the treatment of these conditions.

Clorgyline is a type of medication known as a monoamine oxidase inhibitor (MAOI). It works by blocking the action of an enzyme called monoamine oxidase, which helps to break down certain chemicals in the brain called neurotransmitters. This leads to an increase in the levels of these neurotransmitters in the brain, which can help to improve mood and alleviate symptoms of depression.

Clorgyline is not commonly used as a first-line treatment for depression due to its potential for serious side effects and interactions with certain foods and other medications. It may be used in some cases where other treatments have been unsuccessful, or in research settings to study the role of monoamine oxidase in various physiological processes.

It's important to note that MAOIs like clorgyline require careful monitoring by a healthcare provider and should only be used under close medical supervision due to the risk of serious side effects and interactions.

I'm sorry for any confusion, but "Methyltyrosines" is not a widely recognized medical term or concept in the field of medicine or biochemistry. It seems that there might be some misunderstanding or typo in your question.

If you are referring to "3-Methoxytyrosine" or "3-MT," it is a metabolite of dopamine, which is formed in the body by the enzyme catechol-O-methyltransferase (COMT). 3-MT can be measured in various biological samples, such as urine or plasma, to evaluate the activity of COMT and assess the exposure to drugs that inhibit this enzyme.

If you meant something else by "Methyltyrosines," please provide more context or clarify your question so I can give a more accurate answer.

Drug Information Services (DIS) are specialized resources within healthcare systems, typically staffed by clinical pharmacists and pharmacy residents, that provide evidence-based information and analysis about medications to healthcare professionals and patients. The primary goal of DIS is to optimize medication use and improve patient outcomes through the provision of accurate, unbiased, and timely information on drug therapy.

DIS commonly provide a range of services, including:

1. Answering medication-related questions from healthcare providers, such as physicians, nurses, and other pharmacists, regarding drug interactions, dosing, adverse effects, and therapeutic alternatives.
2. Developing and maintaining formulary management systems to ensure the safe and cost-effective use of medications within a healthcare institution or system.
3. Providing patient education materials and resources on medication therapy, including proper administration techniques, potential side effects, and storage requirements.
4. Conducting ongoing literature evaluations and synthesizing evidence-based recommendations for medication use in various clinical scenarios.
5. Collaborating with healthcare teams to develop and implement guidelines, policies, and procedures related to medication management and safety.
6. Offering educational programs and resources for healthcare professionals and students to enhance their knowledge of pharmacotherapy and medication safety practices.
7. Participating in multidisciplinary committees focused on improving medication use processes, reducing medication errors, and promoting patient safety.

DIS are essential components of modern healthcare systems, as they help ensure the safe, effective, and efficient use of medications for improved patient outcomes.

I'm sorry for any confusion, but "pamphlets" is not a medical term. It refers to a small paper booklet or leaflet that can be used to provide information on various topics, including non-medical subjects. If you have any questions about medical terminology or concepts, I'd be happy to help with those!

Drug labeling refers to the information that is provided on the packaging or container of a medication, as well as any accompanying promotional materials. This information is intended to provide healthcare professionals and patients with accurate and up-to-date data about the drug's composition, intended use, dosage, side effects, contraindications, and other important details that are necessary for safe and effective use.

The labeling of prescription drugs in the United States is regulated by the Food and Drug Administration (FDA), which requires manufacturers to submit proposed labeling as part of their new drug application. The FDA reviews the labeling to ensure that it is truthful, balanced, and not misleading, and provides accurate information about the drug's risks and benefits.

The labeling of over-the-counter (OTC) drugs is also regulated by the FDA, but in this case, the agency has established a set of monographs that specify the conditions under which certain active ingredients can be used and the labeling requirements for each ingredient. Manufacturers of OTC drugs must ensure that their labeling complies with these monographs.

In addition to the information required by regulatory agencies, drug labeling may also include additional information provided by the manufacturer, such as detailed instructions for use, storage requirements, and any warnings or precautions that are necessary to ensure safe and effective use of the medication. It is important for healthcare professionals and patients to carefully review and understand all of the information provided on a drug's labeling before using the medication.

Patient education, as defined by the US National Library of Medicine's Medical Subject Headings (MeSH), is "the teaching or training of patients concerning their own health needs. It includes the patient's understanding of his or her condition and the necessary procedures for self, assisted, or professional care." This encompasses a wide range of activities and interventions aimed at helping patients and their families understand their medical conditions, treatment options, self-care skills, and overall health management. Effective patient education can lead to improved health outcomes, increased patient satisfaction, and better use of healthcare resources.

A formulary is a list of prescription drugs, both generic and brand-name, that are approved for use in a specific health plan or healthcare system. The formulary includes information on the preferred drugs within each therapeutic class, along with any restrictions or limitations on their use. Formularies are developed and maintained by a committee of healthcare professionals, including pharmacists and physicians, who evaluate the safety, efficacy, and cost-effectiveness of different medications.

The purpose of a formulary is to promote the appropriate use of medications, improve patient outcomes, and manage healthcare costs. By establishing a preferred list of drugs, health plans and healthcare systems can negotiate better prices with pharmaceutical manufacturers and ensure that patients receive high-quality, evidence-based care.

Formularies may include various types of medications, such as oral solid dosage forms, injectables, inhalants, topicals, and others. They are typically organized by therapeutic class, and each drug is assigned a tier based on its cost and clinical value. Tier 1 drugs are usually preferred generics or lower-cost brand-name medications, while Tier 2 drugs may be higher-cost brand-name medications that have no generic equivalent. Tier 3 drugs are typically specialty medications that are used to treat complex or rare conditions and are often associated with high costs.

Healthcare providers are encouraged to prescribe drugs that are listed on the formulary, as these medications have been thoroughly reviewed and deemed safe and effective for use in their patient population. However, there may be situations where a non-formulary medication is necessary to treat a particular patient's condition. In such cases, healthcare providers can request an exception or prior authorization to prescribe the non-formulary drug.

Formularies are regularly updated to reflect new drugs that come on the market, changes in clinical guidelines, and shifts in the therapeutic landscape. Health plans and healthcare systems may also modify their formularies in response to feedback from patients and providers or to address concerns about safety, efficacy, or cost.

In summary, a formulary is a comprehensive list of prescription drugs that are approved for use in a specific health plan or healthcare system. Formularies promote the appropriate use of medications, improve patient outcomes, and manage costs by encouraging the prescribing of safe and effective drugs that have been thoroughly reviewed and deemed appropriate for their patient population.

The "drug industry" is also commonly referred to as the "pharmaceutical industry." It is a segment of the healthcare sector that involves the research, development, production, and marketing of medications or drugs. This includes both prescription and over-the-counter medicines used to treat, cure, or prevent diseases and medical conditions in humans and animals.

The drug industry comprises various types of organizations, such as:

1. Research-based pharmaceutical companies: These are large corporations that focus on the research and development (R&D) of new drugs, clinical trials, obtaining regulatory approvals, manufacturing, and marketing their products globally. Examples include Pfizer, Johnson & Johnson, Roche, and Merck.

2. Generic drug manufacturers: After the patent for a brand-name drug expires, generic drug manufacturers can produce and sell a similar version of the drug at a lower cost. These companies must demonstrate that their product is bioequivalent to the brand-name drug in terms of safety, quality, and efficacy.

3. Biotechnology companies: These firms specialize in developing drugs using biotechnological methods, such as recombinant DNA technology, gene therapy, or monoclonal antibodies. Many biotech companies focus on specific therapeutic areas, like oncology, immunology, or neurology.

4. Contract research organizations (CROs): CROs provide various services to the drug industry, including clinical trial management, data analysis, regulatory affairs support, and pharmacovigilance. They work with both large pharmaceutical companies and smaller biotech firms to help streamline the drug development process.

5. Drug delivery system companies: These organizations focus on developing innovative technologies for delivering drugs more effectively and safely to patients. Examples include transdermal patches, inhalers, or long-acting injectables.

6. Wholesalers and distributors: Companies that purchase drugs from manufacturers and distribute them to pharmacies, hospitals, and other healthcare providers.

The drug industry plays a crucial role in improving public health by discovering, developing, and delivering new treatments for various diseases and medical conditions. However, it is also subject to criticism and regulation due to concerns about high drug prices, marketing practices, and the potential for conflicts of interest between industry and healthcare professionals.

A Computerized Medical Record System (CMRS) is a digital version of a patient's paper chart. It contains all of the patient's medical history from multiple providers and can be shared securely between healthcare professionals. A CMRS includes a range of data such as demographics, progress notes, problems, medications, vital signs, past medical history, immunizations, laboratory data, and radiology reports. The system facilitates the storage, retrieval, and exchange of this information in an efficient manner, and can also provide decision support, alerts, reminders, and tools for performing data analysis and creating reports. It is designed to improve the quality, safety, and efficiency of healthcare delivery by providing accurate, up-to-date, and comprehensive information about patients at the point of care.

... is the major metabolite of imipramine and lofepramine. Desipramine is a tricyclic compound, specifically a ... desipramine). Desipramine is a secondary amine TCA, with its N-methylated parent imipramine being a tertiary amine. Other ... Desipramine at very low doses is also used to help reduce the pain associated with functional dyspepsia. It has also been tried ... Desipramine is primarily used for the treatment of depression. It may also be useful to treat symptoms of attention-deficit ...
Christian, Chris (December 1997). "Waiting for God: Desipramine". Sonic Boom. 5 (11). Retrieved July 22, 2020. Desipramine ( ... Aiding & Abetting gave Desipramine a positive review, calling it "much edgier sound than the first album" and saying "the ... Desipramine is the second studio album by Waiting for God, released in 1997 by Synthetic Symphony. ... 1997.{{cite AV media notes}}: CS1 maint: others in cite AV media (notes) (link) Desipramine at Discogs (list of releases) (CS1 ...
"desipramine (Rx) - Norpramin". Medscape Drugs & Diseases. Otasowie, J; Castells, X; Ehimare, UP; Smith, CH (19 September 2014 ... There is good empirical evidence for short-term safety and efficacy for the use of desipramine, bupropion and atomoxetine. ... These include the alpha-2 agonists (clonidine and guanfacine), tricyclic antidepressants (desipramine and nortriptyline), and ... Methylphenidate, guanfacine, clonidine, and desipramine were associated with improvement of tic symptoms. Controversy remains, ...
Comparison of fluvoxamine and desipramine". Arch Gen Psychiatry. 47 (6): 577-85. doi:10.1001/archpsyc.1990.01810180077011. PMID ...
Dean Miles, Larry (1997). "Waiting for God: Desipramine" (PDF). Black Monday (7): 1. Retrieved August 14, 2020. Christian, ...
Hearn L, Moore RA, Derry S, Wiffen PJ, Phillips T (September 2014). Hearn L (ed.). "Desipramine for neuropathic pain in adults ... imapramine, and desipramine,) serotonin-norepinephrine reuptake inhibitor (SNRI) medications (duloxetine, venlafaxine, and ... Cochrane systematically reviewed the evidence for the antidepressants nortriptyline, desipramine, venlafaxine and milnacipran ...
Among the TCAs, amitriptyline is most widely used for this condition, but desipramine and nortriptyline have fewer side effects ... TCAs include imipramine, amitriptyline, desipramine, and nortriptyline. They are generally regarded as first or second-line ...
Other dibenzazepine TCAs include imipramine, desipramine, and clomipramine. Trimipramine is a derivative of imipramine with a ... desipramine, doxepin, imipramine, and trimipramine) were identified. Common adverse effects include: Sedation - especially ...
Examples include imipramine, doxepin, amitriptyline, nortriptyline and desipramine. TCAs may cause drug poisoning in patients ...
Other secondary amine TCAs include desipramine and nortriptyline. The chemical name of protriptyline is 3-(5H-dibenzo[a,d][7] ...
Other secondary amine TCAs include desipramine and protriptyline. The chemical name of nortriptyline is 3-(10,11-dihydro-5H- ... 752-. ISBN 978-3-88763-075-1. "ChemIDplus - 62265-06-9 - AMLRZIZSGSCSHZ-UHFFFAOYSA-N - Desipramine dibudinate - Similar ...
Although lofepramine is technically a tertiary amine, it acts in large part as a prodrug of desipramine, and is more similar to ... The desipramine metabolite is partly secreted in the faeces. Other routes of metabolism include hydroxylation, glucuronidation ... Lofepramine has been said to be a prodrug of desipramine, although there is also evidence against this notion. Lofepramine is ... Lofepramine is a tertiary amine TCA, with its side chain-demethylated metabolite desipramine being a secondary amine. Unlike ...
Zhou Z, Zhen J, Karpowich NK, Goetz RM, Law CJ, Reith ME, Wang DN (September 2007). "LeuT-desipramine structure reveals how ...
... desipramine). Imipramine is a tertiary amine TCA, with its side chain-demethylated metabolite desipramine being a secondary ... Desipramine has more affinity to norepinephrine transporter than imipramine. Dopamine: imipramine blocks D2 receptors. ... Ghanizadeh A (July 2013). "A systematic review of the efficacy and safety of desipramine for treating ADHD". Current Drug ... Blood levels between 150 and 250 ng/mL of imipramine plus its metabolite desipramine generally correspond to antidepressant ...
ISBN 978-1-4051-1071-6. Zhou Z, Zhen J, Karpowich NK, Goetz RM, Law CJ, Reith ME, Wang DN (2007). "LeuT-desipramine structure ...
Zhou Z, Zhen J, Karpowich NK, Goetz RM, Law CJ, Reith ME, Wang DN (September 2007). "LeuT-desipramine structure reveals how ... and that desipramine had no effect on SERT. In a separate experiment, Horschitz et al. exposed HEK-SERT with citalopram on a ... or desipramine (an inhibitor of norepinephrine reuptake protein, NET). By examining the dose-response curves (using a normal ... such as desipramine) and SSRIs. Tricyclic antidepressants inhibit the reuptake of both serotonin and norepinephrine by acting ...
"LeuT-desipramine structure reveals how antidepressants block neurotransmitter reuptake". Science. New York, N.Y. 317 (5843): ...
Nortriptyline, desipramine, and amoxapine are tricyclic antidepressants and secondary amines. (The tricyclics are grouped by ...
Marin, Kocsis, Frances, and Parides (1994) conducted an eight-week open trial that entailed the administration of desipramine ... Marin, D.; Kocsis, J.; Frances, A.; Parides, M. (1994). "Desipramine for the treatment of "pure" dysthymia versus "double" ...
These drugs include amiodarone, desipramine, isoniazid, ketoconazole, letrozole, methoxsalen and tranylcypromine. The ...
It acts primarily as a norepinephrine reuptake inhibitor similarly to desipramine. The synthesis is similar to that reported ...
"The methylphenidate test for differentiating desipramine-responsive from nortriptyline-responsive depression". The American ...
A Double Blind Comparative Trial of Nomifensin and Desipramine in Depression. Relation Between Treatment and Phenylethylamine ...
These include the alpha-2 agonists (clonidine and guanfacine). There is good empirical support for the use of desipramine, ... There is moderate evidence supporting that clonidine combined with methylphenidate, desipramine, and methylphenidate alone ... reduce tics more than placebo when ADHD is also present; desipramine is rarely used following reports of sudden death in ...
Desipramine - may improve working memory and attention when used at certain doses. ISRIB enhanced spatial and fear-associated ...
Desipramine - may improve working memory and attention when used at certain doses. ISRIB enhanced spatial and fear-associated ...
"Pharmacological properties of the active metabolites of the antidepressants desipramine and citalopram". Eur. J. Pharmacol. 576 ...
Norapramin (Desipramine) - an antidepressant, also used in the treatment of nerve pain. Nuplazid (pimavanserin) - an ...
Clinically, quinupramine is reported to be stimulating similarly to imipramine, desipramine, and demexiptiline. It can be ...
Additionally, desipramine, dothiepin, phenelzine, tetrabenazine, and reserpine have been known to trigger NMS. Whether lithium ...
Desipramine is the major metabolite of imipramine and lofepramine. Desipramine is a tricyclic compound, specifically a ... desipramine). Desipramine is a secondary amine TCA, with its N-methylated parent imipramine being a tertiary amine. Other ... Desipramine at very low doses is also used to help reduce the pain associated with functional dyspepsia. It has also been tried ... Desipramine is primarily used for the treatment of depression. It may also be useful to treat symptoms of attention-deficit ...
Desipramine hydrochloride overdose occurs when someone takes more than ... Desipramine hydrochloride is a type of medicine called a tricyclic antidepressant. It is taken to relieve symptoms of ... An overdose of desipramine hydrochloride can be very serious. Complications such as pneumonia, muscle damage from lying on a ... Desipramine hydrochloride is a type of medicine called a tricyclic antidepressant. It is taken to relieve symptoms of ...
DESIPRAMINE, 75MG, TABLET. Common uses. This medication is typically used for depression. It may also be used to assist in the ...
Long-term administration of the tricyclic antidepressant desipramine influences salivary gland function and oral health in ... Long-term administration of the tricyclic antidepressant desipramine influences salivary gland function and oral health in ...
JavaScript is disabled for your browser. Some features of this site may not work without it ...
... HCl A tricyclic dibenzazepine compound that potentiates neurotransmission. Desipramine selectively blocks reuptake ... desipramine 🐶 Veterinary Use , Indications/Contra , FAERs-F , FAERs-M , Orange Bk , BioActivity , Stem definition. Drug id. CAS ... Desipramine Hydrochloride. HUMAN PRESCRIPTION DRUG LABEL. 1. 0781-8218. TABLET, FILM COATED. 10 mg. ORAL. ANDA. 20 sections ... Desipramine Hydrochloride. HUMAN PRESCRIPTION DRUG LABEL. 1. 0781-8218. TABLET, FILM COATED. 10 mg. ORAL. ANDA. 20 sections ...
USES: Desipramine is used to treat depression. This medication may improve your mood, sleep, appetite, and energy level and may ... Therefore, before using desipramine, report all medications you are currently using to your doctor or pharmacist. Also report ... Many drugs besides desipramine may affect the heart rhythm (QT prolongation in the EKG), including amiodarone, dofetilide, ... Talk to your doctor about using desipramine safely. Before having surgery, tell your doctor or dentist that you are taking this ...
Find out what health conditions may be a health risk when taken with Desipramine Oral ... Drugs & MedicationsDesipramine HCL. Who should not take Desipramine HCL?. The following conditions are contraindicated with ... WebMD provides common contraindications for Desipramine Oral. ...
Desipramine (Norpramin) by Dr Jason Cafer MD, Visualize to Memorize 270 Medication Mascots ... Desipramine is an active metabolite of imipramine. In regard to side effects, "desipramine is more desirable than imipramine". ... Desipramine has the weakest antihistamine activity of all TCAs, making it non-sedating. While other TCAs are useful for ... Released in 1963, desipramine (Norpramin) was once commonly prescribed, but is rarely used today. It is exceptionally fatal in ...
... is the hydrochloride salt form of desipramine. In the central nervous system (CNS), desipramine hydrochloride blocks the re- ... Desipramine Hydrochloride a secondary amine tricyclic antidepressant (TCA), ... Desipramine Hydrochloride a secondary amine tricyclic antidepressant (TCA), is the hydrochloride salt form of desipramine. In ... the central nervous system (CNS), desipramine hydrochloride blocks the re-uptake of neurotransmitters, including norepinephrine ...
Desipramine (Norpramin). *View full drug information. May increase synaptic concentration of norepinephrine in CNS by ...
Round and has been identified as Desipramine Hydrochloride 150 mg. It is supplied by Amide Pharmaceutical Inc. ... Desipramine Hydrochloride. Imprint. E 760. Strength. 150 mg. Color. White. Size. 11.00 mm. Shape. Round. Availability. ... Desipramine is used in the treatment of Depression and belongs to the drug class tricyclic antidepressants. FDA has not ... Pill with imprint E 760 is White, Round and has been identified as Desipramine Hydrochloride 150 mg. It is supplied by Amide ...
Since 2010, Ingenus has developed, manufactured and commercialized quality generic medications as cost effective solutions for patients, suppliers and stakeholders across the healthcare continuum. Ingenus has improved patient access, offset healthcare costs and maintained high quality standards that we have become known for ...
encoded search term (Desipramine Level) and Desipramine Level What to Read Next on Medscape ... Desipramine Level Updated: Jan 16, 2014 * Author: Bishnu Prasad Devkota, MD, MHI, FRCS(Edin), FRCS(Glasg), FACP; Chief Editor: ... 4] Desipramine has been found useful in the therapy of irritable bowel syndrome (IBS). Empiric evidence for efficacy of its use ... Desipramine falls in the broad group of tricyclic antidepressants (TCA). Currently, it is used primarily in depression that is ...
encoded search term (Desipramine Level) and Desipramine Level What to Read Next on Medscape ... Desipramine Level Updated: Jan 16, 2014 * Author: Bishnu Prasad Devkota, MD, MHI, FRCS(Edin), FRCS(Glasg), FACP; Chief Editor: ... 4] Desipramine has been found useful in the therapy of irritable bowel syndrome (IBS). Empiric evidence for efficacy of its use ... Desipramine falls in the broad group of tricyclic antidepressants (TCA). Currently, it is used primarily in depression that is ...
desipramine (Norpramin ®). desvenlafaxine (Khedezla®, Pristiq®). doxepin (Sinequan ®). duloxetine (Cymbalta ® ). escitalopram ( ...
Desipramine: an antidepressant that increases levels of the neurotransmitter norepinephrine in the brain ...
desipramine. 2D6 sensitive substrate. dextromethorphan. 2D6 sensitive substrate. diazepam. 2C19 moderate sensitive substrate. ...
Brisdelle (paroxetine) is a prescription capsule used to treat moderate to severe hot flashes due to menopause. Learn about side effects and more.
Indeed, vacuolin-1 or desipramine treatment prevented the enhancement of CME but not of fluid phase endocytosis upon USMB, ... desipramine treatment alone had no effect on fluid-phase endocytosis (Fig 9A-9C), suggesting that desipramine synergizes with ... Ho C-M, Kuo S-Y, Chen C-H, Huang J-K, Jan C-R (2005) Effect of desipramine on Ca2+ levels and growth in renal tubular cells. ... Desipramine Inhibits the USMB-Stimulated Reduction of Cell Surface TfR. In response to membrane damage by SLO, cells undergo ...
This medicine comes with a patient information insert. Read and follow these instructions carefully. Ask your doctor or pharmacist if you have any questions. The solution comes in small containers that are only used one time. Throw the empty container away after putting the medicine into your ear(s). This medicine should be used only inside the ear. Do not put it in the eyes or nose, and do not take it by mouth. If this medicine is swallowed by accident or gets into your eyes, call your doctor right away. It is important that the infected ear remain clean and dry. When bathing, avoid getting the infected ear wet. Avoid swimming unless your doctor has instructed you otherwise. To use the ear drops:. ...
Detailed drug Information for Pancof HC. Includes common brand names, drug descriptions, warnings, side effects and dosing information.
Check with your doctor right away if you have pain or tenderness in the upper stomach, pale stools, dark urine, loss of appetite, nausea, vomiting, unusual tiredness or weakness, or yellow eyes or skin. These could be symptoms of a serious liver problem. This medicine may cause serious lung or breathing problems (eg, interstitial lung disease, pneumonitis). Check with your doctor right away if you have chest pain, chills, cough, fever, general feeling of discomfort or illness, thickening of bronchial secretions, or trouble breathing. Check with your doctor right away if blurred vision, dizziness, nervousness, headache, pounding in the ears, or slow or fast heartbeat occurs during or after treatment with this medicine. These can be symptoms of hypertension (high blood pressure). This medicine can cause changes in your heart rhythm, including a condition called QT prolongation. Call your doctor right away if you have dizziness, fainting, or slow, fast, pounding, or uneven heartbeats. This medicine ...
Desipramine. 25-200 mg/d. Use with caution in elderly patients.. [33][Level of evidence: III]. ...
Desipramine. A single STENDRA 200 mg dose increased AUC and Cmax of a single 50 mg dose of desipramine, a CYP2D6 substrate, by ... Omeprazole, Rosiglitazone, and Desipramine. The effect of avanafil on the pharmacokinetics of omeprazole (a CYP2C19 substrate ... Co-administration with avanafil resulted in an approximate 5.7% increase in AUC0-inf and 5.2% increase in Cmax of desipramine. ... Twenty healthy male volunteers received a single 50 mg desipramine tablet then a single 200 mg avanafil tablet 2 hours after ...
The pA2 values were: amitriptyline 7.4; doxepin 6.8; desipramine 5.9; dibenzopine 508; protriptyline 5.7; and iprindole 5.5. ...
  • Desipramine, sold under the brand name Norpramin among others, is a tricyclic antidepressant (TCA) used in the treatment of depression. (wikipedia.org)
  • Desipramine hydrochloride is found in the medicine called Norpramin. (medlineplus.gov)
  • Released in 1963, desipramine (Norpramin) was once commonly prescribed, but is rarely used today. (cafermed.com)
  • Desipramine is the generic name of the drug and its INNTooltip International Nonproprietary Name and BANTooltip British Approved Name, while desipramine hydrochloride is its USANTooltip United States Adopted Name, USPTooltip United States Pharmacopeia, BANTooltip British Approved Name, and JANTooltip Japanese Accepted Name. (wikipedia.org)
  • Desipramine hydrochloride is a type of medicine called a tricyclic antidepressant. (medlineplus.gov)
  • Desipramine hydrochloride overdose occurs when someone takes more than the normal or recommended amount of this medicine. (medlineplus.gov)
  • Below are symptoms of a desipramine hydrochloride overdose in different parts of the body. (medlineplus.gov)
  • An overdose of desipramine hydrochloride can be very serious. (medlineplus.gov)
  • Desipramine Hydrochloride a secondary amine tricyclic antidepressant (TCA), is the hydrochloride salt form of desipramine. (scientist.com)
  • In the central nervous system (CNS), desipramine hydrochloride blocks the re-uptake of neurotransmitters, including norepinephrine and serotonin. (scientist.com)
  • Pill with imprint E 760 is White, Round and has been identified as Desipramine Hydrochloride 150 mg. (drugs.com)
  • To determine whether elevations of plasma norepinephrine (NE) in major depression represent increased sympathetic nervous system (SNS) activity and to assess the effects of desipramine hydrochloride on sympathetic function. (jamanetwork.com)
  • Secondary amine TCAs like desipramine and nortriptyline have a lower risk of orthostatic hypotension than other TCAs, although desipramine can still cause moderate orthostatic hypotension. (wikipedia.org)
  • Desipramine (and nortriptyline) have been referred to as second generation TCAs, making imipramine (and amitriptyline) first generations. (cafermed.com)
  • Desipramine is the major metabolite of imipramine and lofepramine. (wikipedia.org)
  • Other dibenzazepine TCAs include imipramine (N-methyldesipramine), clomipramine, trimipramine, and lofepramine (N-(4-chlorobenzoylmethyl)desipramine). (wikipedia.org)
  • Desipramine is a secondary amine TCA, with its N-methylated parent imipramine being a tertiary amine. (wikipedia.org)
  • Desipramine is an active metabolite of imipramine. (cafermed.com)
  • Desipramine has the weakest antihistamine and anticholinergic effects of the TCAs. (wikipedia.org)
  • Desipramine has the weakest antihistamine activity of all TCAs, making it non-sedating. (cafermed.com)
  • Desipramine is used in the treatment of Depression and belongs to the drug class tricyclic antidepressants . (drugs.com)
  • Desipramine falls in the broad group of tricyclic antidepressants (TCA). (medscape.com)
  • Unlike most other TCAs, desipramine causes no weight gain, sexual dysfunction, or orthostatic hypotension. (cafermed.com)
  • Desipramine is particularly toxic in cases of overdose, compared to other antidepressants. (wikipedia.org)
  • Any overdose or suspected overdose of desipramine is considered to be a medical emergency and can result in death without prompt medical intervention. (wikipedia.org)
  • The main disadvantage of desipramine is risk of mortality in single-dose overdose, which appears to be higher than any other antidepressant. (cafermed.com)
  • Desipramine levels are increased in overdose. (medscape.com)
  • Desipramine tends to be less sedating than other TCAs and tends to produce fewer anticholinergic effects such as dry mouth, constipation, urinary retention, blurred vision, and cognitive or memory impairments. (wikipedia.org)
  • Whereas other TCAs are useful for treating insomnia, desipramine can cause insomnia as a side effect due to its activating properties. (wikipedia.org)
  • While other TCAs are useful for treating insomnia, desipramine can cause insomnia. (cafermed.com)
  • Desipramine is primarily used for the treatment of depression. (wikipedia.org)
  • Desipramine is used to treat depression. (healthwarehouse.com)
  • Sympathetic nervous system activity is elevated in major depression and is suppressed by short-term desipramine administration. (jamanetwork.com)
  • Response to desipramine treatment in adolescent depression: a fixed-dose, placebo controlled trial. (bvsalud.org)
  • Desipramine is a very potent and relatively selective norepinephrine reuptake inhibitor (NRI), which is thought to enhance noradrenergic neurotransmission. (wikipedia.org)
  • Desipramine selectively blocks reuptake of norepinephrine from the neural synapse, and also appears to impair serotonin transport. (drugcentral.org)
  • Desipramine is a tricyclic compound, specifically a dibenzazepine, and possesses three rings fused together with a side chain attached in its chemical structure. (wikipedia.org)
  • The observed effectiveness of desipramine in the treatment of ADHD was the basis for the development of the selective NRI atomoxetine and its use in ADHD. (wikipedia.org)
  • The observation that desipramine helped ADHD was the basis for development of the NRI atomoxetine (Strattera). (cafermed.com)
  • Indeed, vacuolin-1 or desipramine treatment prevented the enhancement of CME but not of fluid phase endocytosis upon USMB, suggesting that lysosome exocytosis and acid sphingomyelinase, respectively, are required for the regulation of CME but not fluid phase endocytosis upon USMB treatment. (plos.org)
  • The initial suppression of SNS activity by desipramine was reversed by long-term (28 days) treatment of patients, with extravascular and vascular NE appearance rates returning to approximately basal levels. (jamanetwork.com)
  • The demonstration of SNS reactivation occurring with prolonged desipramine treatment is compatible with the theory that long-term treatment desensitizes CNS α 2 -adrenergic receptors and emphasizes the value of examining the temporal course of responses to pharmacological challenges of neuroendocrine systems. (jamanetwork.com)
  • Using in situ hybridization, we examined the effects of chronic treatment with fluoxetine (FLU) or desipramine (DMI) on BDNF, CaMKKalpha and CaMKKbeta mRNAs in the hippocampus of wild-type (Wt) and transgenic (TG) mice characterized by glucocorticoid receptor (GR) dysfunction. (unimore.it)
  • Desipramine 150 mg is not a controlled substance under the Controlled Substances Act (CSA). (drugs.com)
  • On drug screens, desipramine can cause a false positive for amphetamine or LSD. (cafermed.com)
  • [ 4 ] Desipramine has been found useful in the therapy of irritable bowel syndrome (IBS). (medscape.com)
  • Desipramine, given for 2 days, significantly reduced the concentration of NE in plasma of patients and controls by markedly suppressing the rates of extravascular and vascular NE appearance, compatible with a short-term reduction in SNS activity. (jamanetwork.com)
  • Desipramine at very low doses is also used to help reduce the pain associated with functional dyspepsia. (wikipedia.org)
  • Desipramine is a tricyclic antidepressant (TCA). (medscape.com)
  • Desipramine hydrochloride is a type of medicine called a tricyclic antidepressant. (nih.gov)
  • Desipramine is an oral tricyclic antidepressant that widely used in the therapy of depression. (nih.gov)
  • To determine whether clomipramine hydrochloride, a serotonin reuptake blocker with unique antiobsessional properties, is differentially effective for obsessivecompulsive and stereotyped motor behaviors in autistic disorder compared with placebo and with the noradrenergic tricyclic antidepressant agent, desipramine hydrochloride. (jamanetwork.com)
  • A small number of children, teenagers, and young adults (up to 24 years of age) who took antidepressants ('mood elevators') such as desipramine during clinical studies became suicidal (thinking about harming or killing oneself or planning or trying to do so). (medlineplus.gov)
  • You should know that your mental health may change in unexpected ways when you take desipramine or other antidepressants even if you are an adult over age 24. (medlineplus.gov)
  • Desipramine is in a class of medications called tricyclic antidepressants. (medlineplus.gov)
  • Desipramine is particularly toxic in cases of overdose, compared to other antidepressants. (wikipedia.org)
  • Evidence indicates that the secondary amine tricyclic antidepressants, including desipramine hydrochloride, may have greater activity in blocking the re-uptake of norepinephrine. (nih.gov)
  • Tricyclic antidepressants, such as desipramine hydrochloride, are rapidly absorbed from the gastrointestinal tract. (nih.gov)
  • Desipramine falls in the broad group of tricyclic antidepressants (TCA). (medscape.com)
  • Desipramine overdose is more likely to result in death than overdose with other tricyclic antidepressants, notes a company letter sent to healthcare professionals. (medscape.com)
  • Desipramine belongs to the class of medications known as tricyclic antidepressants . (pharmachoice.com)
  • Tricyclic antidepressants such as desipramine work by increasing the amount of norepinephrine and serotonin neurotransmitters (chemical substances in the brain) available in certain parts of the brain. (pharmachoice.com)
  • Following a 2-week, single-blind placebo washout phase, 12 autistic subjects completed a 10week, double-blind, crossover comparison of clomipramine and placebo, and 12 different subjects completed a similar comparison of clomipramine and desipramine. (jamanetwork.com)
  • Clomipramine was equal to desipramine and both tricyclic agents were superior to placebo for amelioration of hyperactivity. (jamanetwork.com)
  • Anyone considering the use of desipramine hydrochloride tablets or any other antidepressant in a child, adolescent, or young adult must balance this risk with the clinical need. (nih.gov)
  • Your doctor may start you on a low dose of desipramine and gradually increase your dose. (medlineplus.gov)
  • Up to a 36-fold difference in plasma level may be noted among individuals taking the same oral dose of desipramine. (nih.gov)
  • There are documented clinical drug-drug interactions between bupropion and the CYP2D6-metabolized drug desipramine resulting in marked (5-fold) increases in desipramine exposure. (aspetjournals.org)
  • Using the in vitro kinetic constants and estimated liver concentrations of bupropion and its metabolites, modeling was able to predict within 2-fold the increase in desipramine exposure observed when coadministered with bupropion. (aspetjournals.org)
  • This work indicates that the reductive metabolites of bupropion are potent competitive CYP2D6 inhibitors in vivo and provides a mechanistic explanation for the clinical drug-drug interaction between bupropion and desipramine. (aspetjournals.org)
  • Desipramine hydrochloride, USP is an antidepressant drug of the tricyclic type available as tablets of 10 mg, 25 mg, 50 mg, 75 mg, 100 mg, or 150 mg for oral administration. (nih.gov)
  • Forced swimming test in rats: Effect of desipramine administration and the period of exposure to the test on struggling behavior, swimming, immobility and defecation rate. (bvsalud.org)
  • Effects of desipramine on clinical liver function tests. (nih.gov)
  • Utility of crossover designs in clinical trials: efficacy of desipramine vs. placebo in opioid-dependent cocaine abusers. (uams.edu)
  • 05), with no differences between desipramine and placebo. (jamanetwork.com)
  • The effects of desvenlafaxine and paroxetine on the pharmacokinetics of the cytochrome P450 2D6 substrate desipramine in healthy adults. (cdc.gov)
  • A literature review by Pérez-López et al indicated that in women with vestibulodynia, treatment with oral desipramine, with or without topical lidocaine, can lead to significant improvement in the Index of Sexual Satisfaction score, as assessed by the investigators through network meta-analyses. (medscape.com)
  • If you suddenly stop taking desipramine, you may experience withdrawal symptoms such as nausea, headache, and weakness. (medlineplus.gov)
  • Finally, an old warning that "physostigmine is not recommended except to treat life-threatening symptoms" and a recommendation that "plasma desipramine measurements are best for dosage monitoring" have both now been removed from the labeling altogether. (medscape.com)
  • Children younger than 18 years of age should not normally take desipramine, but in some cases, a doctor may decide that desipramine is the best medication to treat a child's condition. (medlineplus.gov)
  • The doctor or pharmacist will give you the manufacturer's patient information sheet (Medication Guide) when you begin treatment with desipramine. (medlineplus.gov)
  • Desipramine is a very potent and relatively selective norepinephrine reuptake inhibitor (NRI), which is thought to enhance noradrenergic neurotransmission. (wikipedia.org)
  • Adverse events and deaths related to desipramine should be reported to MedWatch by telephone at 1-800-FDA-1088, by fax at 1-800-FDA-0178, online at https://www.fda.gov/medwatch , or by mail to 5600 Fishers Lane, Rockville, Maryland 20852-9787. (medscape.com)
  • Desipramine is metabolized in the liver, and approximately 70% is excreted in the urine. (nih.gov)
  • Desipramine can cause mild and transient serum enzyme elevations and is rare cause of clinically apparent acute cholestatic liver injury. (nih.gov)
  • Desipramine is the generic name of the drug and its INNTooltip International Nonproprietary Name and BANTooltip British Approved Name, while desipramine hydrochloride is its USANTooltip United States Adopted Name, USPTooltip United States Pharmacopeia, BANTooltip British Approved Name, and JANTooltip Japanese Accepted Name. (wikipedia.org)
  • Individuals taking desipramine were successfully switched to amitriptyli. (echeat.com)
  • desipramine increases effects of vasopressin by pharmacodynamic synergism. (medscape.com)
  • It may take 2 to 3 weeks for you to feel the full benefit of desipramine. (medlineplus.gov)
  • Beschreibung Desipramine.HCl Product reference number DSP-1093-HC Full chemical name 3-(10,11-Dihydro-5H-dibenzo[b,f]azepin-5-yl)-N-methylpropan-1-amine.hydrochloride Formula C18H22N2.HCl Molecular weight 302.84 CAS Number 58-28-6 Supplied a. (lipomed-shop.com)
  • The chemical name of desipramine is 3-(10,11-dihydro-5H-dibenzo[b,f]azepin-5-yl)-N-methylpropan-1-amine and its free base form has a chemical formula of C18H22N2 with a molecular weight of 266.381 g/mol. (wikipedia.org)