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Anxiolytics metabolism

As to be expected from a peptide that has been highly conserved during evolution, NPY has many effects, e.g. in the central and peripheral nervous system, in the cardiovascular, metabolic and reproductive system. Central effects include a potent stimulation of food intake and appetite control [2], anxiolytic effects, anti-seizure activity and various forms of neuroendocrine modulation. In the central and peripheral nervous system NPY receptors (mostly Y2 subtype) mediate prejunctional inhibition of neurotransmitter release. In the periphery NPY is a potent direct vasoconstrictor, and it potentiates vasoconstriction by other agents (mostly via Yi receptors) despite reductions of renal blood flow, NPY enhances diuresis and natriuresis. NPY can inhibit pancreatic insulin release and inhibit lipolysis in adipocytes. It also can regulate gut motility and gastrointestinal and renal epithelial secretion. [Pg.829]

Zolpidem, chemically unrelated to benzodiazepines or barbiturates, acts selectively at the y-aminobutyric acidA (GABAA)-receptor and has minimal anxiolytic and no muscle relaxant or anticonvulsant effects. It is comparable in effectiveness to benzodiazepine hypnotics, and it has little effect on sleep stages. Its duration is approximately 6 to 8 hours, and it is metabolized to inactive metabolites. Common side effects are drowsiness, amnesia, dizziness, headache, and GI complaints. Rebound effects when discontinued and tolerance with prolonged use are minimal, but theoretical concerns about abuse exist. It appears to have minimal effects on next-day psychomotor performance. The usual dose is 10 mg (5 mg in the elderly or those with liver impairment), which can be increased up to 20 mg nightly. Cases of psychotic reactions and sleep-eating have been reported. [Pg.830]

Examples of monoamine oxidase inhibitors are phenelzine, tranylcypromine, isocarboxazid and mo-clobemide. They are indicated for atypical depression. Changes in the neurotransmitter levels are seen in several days but the clinical effect may lag by several weeks. Phenelzine is a non-selective hydrazine-type monoamine oxidase inhibitor while the also non-selective inhibitor tranylcypromine is of the non-hydrazine-type. Phenelzine, tranylcypromine and isocarboxazid are irreversible inhibitors. Phenelzine is partly metabolized by acetylation and slow acetylators are more prone to toxicity. It has anxiolytic properties and superior efficiacy in treating severe anxiety. [Pg.354]

Abstract Pharmacogenetics as a field of research is increasing the basis of knowledge on the use of psychotropics in different ethnic patient populations. This chapter summarizes cur-rentknowledge on the metabolism of anxiolytic agents with emphasis on pharmacogenetics and ethnic variations in drug responses. [Pg.433]

Pharmacology has provided powerful tools to characterize the neurochemical pathways of stress and anxiety in the brain, and how these pathways are involved in the pathophysiology and treatment of anxiety disorders. In the past, this work has largely focused on classical neurotransmitter systems, including the synthesis, release, and metabolism of monoamines and receptor subtypes that control presynaptic release of neurotransmitters and their postsynaptic effects. Increasing the specihcity of drugs but also the combination of mechanisms has been pursued to improve anxiolytic drugs. [Pg.504]

Table 1 Cytochrome P450 (CYP) isoenzymes and metabolism of antidepressant and anxiolytic drugs and important inhibitors and inductors... Table 1 Cytochrome P450 (CYP) isoenzymes and metabolism of antidepressant and anxiolytic drugs and important inhibitors and inductors...
Chouinard, G., Lefko-Singh, K., and Teboul, E. (1999) Metabolism of anxiolytics and hypnotics benzodiazepines, buspirone, zopli-cone, and zolpidem. Cell Mol Neurobiol 19 533—552. [Pg.350]

Further evidence concerning anxiolytic effects of neurosteroids involves its action on the prefrontal cortical dopamine system. This system has been identified as one of the neuroanatomically involved CNS areas in stress and anxiety responses, where increases in dopamine metabolism are observed following a variety of stressors [A. Y. Deutch and Roth 1990]. Grobin et al. [1992] demonstrated that intracerebroventricularly administered allo-THDOC effectively reduced dopamine metabolism in rats, thereby antagonizing stress-induced activation of the prefrontal cortical dopamine innervation. [Pg.447]

A further issue is raised with regard to dose-dependent effects, suggesting dual or U-shaped psychotropic responses, because recent studies have indicated that neurosteroids may induce anxiogenic or anxiolytic responses in relation to the dosage used and subsequent metabolizing steps involved [Melchior and Ritzmann 1994a, 1994b]. [Pg.448]

Beta-adrenoceptor antagonists, particularly propranolol, have been shown to be effective for anxiety symptoms particularly in situational anxiety and GAD. Buspirone, an azaspirodecanedione, is an agonist at 5-HTlA receptors and seems to have anxiolytic effects, though it is less potent than the BDZs and the effects take up to three weeks to become evident. There is high first pass metabolism and a considerable proportion of the effect is due to a metabolite (1-PP). The principal adverse effects of buspirone are nausea, gastrointestinal upset and headache. Antidepressant drugs, both the older tricyclic antidepressants and the newer drugs, have been demonstrated to have anxiolytic effects in mixed anxiety-depressive patients, GAD and panic disorder. [Pg.173]

Long term or excessive use of these medications may also cause tolerance and physical dependence.14,31 In particular, carisoprodol should be used cautiously because this drug is metabolized in the body to form meprobamate, which is a controlled substance (see Chapter 1) that has sedative/anxiolytic properties but is not used extensively because it has strong potential for abuse.13,73 Hence, use of cariso-... [Pg.166]


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See also in sourсe #XX -- [ Pg.623 , Pg.623 ]




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