Pathways

Amiodarone is a class III antiarrhythmic drug used for treating ventricular arrythmias. It is administered orally or intravenously. Amiodarone targets the cardiac myocytes where it blocks the inward rectifying potassium channels. This potassium is responsible for phase 3 of the action potential. During phase 3, K+ goes out of the cell to allow repolarization. In the presence of amiodarone, K+ accumulates in the cell since the potassium channels are blocked by amiodarone. This causes the repolarization phase, and thus, the action potential duration to be prolonged. The excitability of the cell is reduced and this leads to a slowing of the heart rate. The QRS duration is increased and the QT interval is also prolonged. These effects on the action potentials and the heart rate therefore mean that abnormal heart rhythms like tachyarrhythmias are less likely to occur. Amiodarone may have adverse effects such as thyrotoxicosis or hypothyroidism, tremor, uncontrollable and unusual movement of the body, dizziness, headache, nausea and vomiting, constipation, blurred vision, due to its effects on other targets such as beta-adrenergic receptors, sodium channels, and calcium channels.

Amisulpride, a substituted benzamide derivative, is a second-generation (atypical) antipsychotic. Amisulpride is a selective dopamine D2 and D3 receptor antagonist with no affinity towards other dopamine receptor subtypes. At low doses, it enhances dopaminergic neurotransmission by preferentially blocking presynaptic dopamine D2/D3 autoreceptors. At higher doses, amisupride antagonises postsynaptic dopamine D2 and D3 receptors, preferentially in the limbic system rather than the striatum, thereby reducing dopaminergic transmission.

Metabolites of Amisulpride are predicted with biotransformer.

Amisulpride, a substituted benzamide derivative, is a second-generation (atypical) antipsychotic. Amisulpride is a selective dopamine D2 and D3 receptor antagonist with no affinity towards other dopamine receptor subtypes. At low doses, it enhances dopaminergic neurotransmission by preferentially blocking presynaptic dopamine D2/D3 autoreceptors. At higher doses, amisupride antagonises postsynaptic dopamine D2 and D3 receptors, preferentially in the limbic system rather than the striatum, thereby reducing dopaminergic transmission.

Amitriptyline is a tricyclic antidepressant indicated in the treatment of depressive illness, either endogenous or psychotic, and to relieve depression associated anxiety. The non-FDA-approved indications are anxiety, post-traumatic stress disorder, insomnia, chronic pain (diabetic neuropathy, fibromyalgia), irritable bowel syndrome, interstitial cystitis (bladder pain syndrome), migraine prophylaxis, postherpetic neuralgia, and sialorrhea. The three-ring central structure, along with a side chain, is the basic structure of tricyclic antidepressants. The monoamine hypothesis in depression, one of the oldest hypotheses, postulates that deficiencies of serotonin (5-HT) and/or norepinephrine (NE) neurotransmission in the brain lead to depressive effects. Amitriptyline by blocking the reuptake of both serotonin and norepinephrine neurotransmitters. In adrenergic neurons, norepinephrine is synthesized from tyrosine and stored in synaptic vesicles. Once an action potential arrives at the nerve terminal, calcium channels open, causing the influx of calcium in the cytosol. Calcium then triggers the release of neurotransmitters stored in synaptic vesicles via exocytosis. The norepinephrine is released into the synapse and acts on α1, β1 and β2receptors which contribute to mood improvements. The norepinephrine in the synapse is rapidly taken up by the norepinephrine reuptake transporter on the presynaptic neuron, and is recycled. Amitriptyline inhibits these reuptake transporters on adrenergic neurons, thereby increasing norepinephrine concentration in the synapse. This allows more stimulation of adrenergic needed to improve depressive moods. The most commonly encountered side effects of amitriptyline include weight gain, gastrointestinal symptoms like constipation, xerostomia, dizziness, headache, and somnolence.

Amitriptyline is a tricyclic antidepressant indicated in the treatment of depressive illness, either endogenous or psychotic, and to relieve depression associated anxiety. The non-FDA-approved indications are anxiety, post-traumatic stress disorder, insomnia, chronic pain (diabetic neuropathy, fibromyalgia), irritable bowel syndrome, interstitial cystitis (bladder pain syndrome), migraine prophylaxis, postherpetic neuralgia, and sialorrhea. The three-ring central structure, along with a side chain, is the basic structure of tricyclic antidepressants. The monoamine hypothesis in depression, one of the oldest hypotheses, postulates that deficiencies of serotonin (5-HT) and/or norepinephrine (NE) neurotransmission in the brain lead to depressive effects. Amitriptyline by blocking the reuptake of both serotonin and norepinephrine neurotransmitters. In serotonergic neurons, serotonin is synthesized from tryptophan and stored in synaptic vesicles. Once an action potential arrives at the nerve terminal, calcium channels open, causing the influx of calcium in the cytosol. Calcium then triggers the release of neurotransmitters stored in synaptic vesicles via exocytosis. The serotonin is released into the synapse and acts on 5HT2A and 5HT2C receptors which are responsible for mood improvements. The serotonin in the synapse is rapidly taken up by the serotonin reuptake transporter on the presynaptic neuron, and is recycled. Amitriptyline inhibits these reuptake transporters on serotonergic neurons, thereby increasing serotonin concentration in the synapse. This allows more stimulation of 5HT2A and 5HT2C receptors needed to improve depressive moods.

Amitriptylinoxide is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Amitriptylinoxide passes through the liver and is then excreted from the body mainly through the kidney.