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Reserpine metabolism

Experiments of this kind have provided a great deal of evidence in favour of exocytotic release of vesicular noradrenaline. For example, by administering reserpine (which causes noradrenaline to leak out of the vesicles into the cytoplasm) together with an inhibitor of the enzyme monoamine oxidase (which will prevent metabolism of cytoplasmic noradrenaline), it is possible to redistribute the noradrenaline stored within nerve terminals because it leaks from the vesicles but is preserved within the neuronal cytoplasm. Under these conditions, the total amount of transmitter in the terminals is unchanged but impulse-evoked release rapidly diminishes. [Pg.93]

The Rauwolfia alkaloid reserpine, due to its strong central component of activity, is excluded from this review, even though it has the peripheral effect of releasing norepinephrine from storage sites where it can be metabolized by monoamine oxidase. This results in neurotransmitter depletion and it appears that good blood pressure control would be achieved by a drug which has this peripheral mechanism but lacks the central component. The Mead-Johnson compound MJ-10459-2 (LXI) shows activity in... [Pg.70]

Urine catecholamines may also serve as biomarkers of disulfoton exposure. No human data are available to support this, but limited animal data provide some evidence of this. Disulfoton exposure caused a 173% and 313% increase in urinary noradrenaline and adrenaline levels in female rats, respectively, within 72 hours of exposure (Brzezinski 1969). The major metabolite of catecholamine metabolism, HMMA, was also detected in the urine from rats given acute doses of disulfoton (Wysocka-Paruszewska 1971). Because organophosphates other than disulfoton can cause an accumulation of acetylcholine at nerve synapses, these chemical compounds may also cause a release of catecholamines from the adrenals and the nervous system. In addition, increased blood and urine catecholamines can be associated with overstimulation of the adrenal medulla and/or the sympathetic neurons by excitement/stress or sympathomimetic drugs, and other chemical compounds such as reserpine, carbon tetrachloride, carbon disulfide, DDT, and monoamine oxidase inhibitors (MAO) inhibitors (Brzezinski 1969). For these reasons, a change in catecholamine levels is not a specific indicator of disulfoton exposure. [Pg.122]

Bagdy G, Perenyi A, Frecska E, Seregi A, Fekete MI, Tothfalusi L, Magyar K, Bela A, Arato M. (1988). Effect of adjuvant reserpine treatment on catecholamine metabolism in schizophrenic patients under long-term neuroleptic treatment. J Neural Transm. 71(1) 73-78. [Pg.504]

In addition to drugs administered specifically to produce a metabolic effect, there are drug-related physiological changes that cause laboratory test abnormalities. Many drugs have been associated with the appearance of abnormal liver function tests in a fashion that simulates extrahepatic obstruction. These drugs include, among others, chlorpromazine, cinco-phen, methyltestosterone, thiouracil, p-aminosalicylic acid, sulfadiazine, reserpine, meprobromate, novobiocin, caffeine, and phenacemide (L7, L8, S6). [Pg.21]

C. Amphetamine is an indirectly acting adrenomimetic amine that depends on the release of norepinephrine from noradrenergic nerves for its action. Tlius, its effect depends on neuronal uptake (blocked by cocaine) to displace norepinephrine from the vesicles and the availability of norepinephrine (depleted by reserpine). The substitution on the a-carbon atom blocks oxidation by monoamine oxidase. With no substitution on its benzene ring, amphetamine resists metabolism by COMT. [Pg.107]

Conversely, certain drugs modify the effectiveness or side effects of aspirin. Phenobarbital, occasionally used for seizures, induces liver enzymes that increase the metabolism and excretion of aspirin, (3-adrenoceptorblocking drugs, such as propranolol, and decrease the antiinflammatory effects of aspirin, whereas reserpine decreases its analgesic effects. Antacids decrease the absorption of aspirin. Alcohol consumption in combination with aspirin increases the latter s ulcerogenic effects. [Pg.314]

It therefore appears that the main action of reserpine is to produce a biochemical change so that the cells no longer retain a high concentration of serotonin. In other words, the binding of serotonin is prevented. Thus, after the administration of 5-hydroxytryptophan (a precursor of serotonin) to rabbits pretreated with reserpine, serotonin is rapidly formed but remains in a free form. Presumably, free serotonin, before it is metabolized to 5-hydroxyindole acetic acid by amine... [Pg.517]

J.M. Rand and H. Jurevics "Metabolism of Reserpine" in "Antihypertensive Agents", Ed.F. Gross, Springer-verlag, (1977). [Pg.765]

In contrast to the oxidative reactions discussed above, the only reported biotransformations of reserpine (21) and rescinnamine (23) (42-44) appear to involve hydrolytic processes. Reserpine is readily metabolized by liver homogenates from the mouse (43), rat, guinea pig, dog, and cat (44) to yield methyl reserpate (22) and 3,4,5-trimethoxybenzoic acid in yields of up to 70% (43). The use of reserpine labeled with tritium in the 2 and 6 positions of the trimethoxybenzoate residue indicated that no significant metabolism of reserpine by another route occurred before hydrolysis, reserpine and 3,4,5-trimethoxybenzoic acid being the only detectable radioactive components of the incubation mixture at the conclusion of the reaction (44). An... [Pg.336]

Vincamine is an alkaloid extracted from the plant Vinca minor. Ethyl apovincaminate is a related synthetic ethyl ester of vincaminic acid. These drugs have spasmolytic effects similar to those of reserpine, but also have metabolic effects, including, in high doses, inhibition of phosphodiesterase. Although increased cerebral blood flow has been reported after the intravenous administration of vincamine, there have been no reliable studies of blood flow after oral medication. Improvement in scores on some psychometric tests have been obtained in some patients with cerebrovascular disease, but no clear-cut practical benefit has been demonstrated. [Pg.3641]

Reserpine is absorbed rapidly after oral administration. Fat tissue accumulates rc.serpinc slowly, with a maximal level reached between 4 and 6 hours. After 24 hours, small amounts of reserpine are found in the liver and fat. but none is found in the brain or other tissues. Re.serpine is metabolized by the liver and intestine to methyl re.serpatc and. 1.4.S-trimcthoxybenzoic acid. [Pg.650]


See other pages where Reserpine metabolism is mentioned: [Pg.337]    [Pg.197]    [Pg.337]    [Pg.197]    [Pg.47]    [Pg.171]    [Pg.305]    [Pg.32]    [Pg.193]    [Pg.195]    [Pg.220]    [Pg.314]    [Pg.234]    [Pg.26]    [Pg.118]    [Pg.221]    [Pg.877]    [Pg.455]    [Pg.687]    [Pg.741]    [Pg.1200]    [Pg.1789]    [Pg.1216]    [Pg.518]    [Pg.496]    [Pg.757]    [Pg.131]    [Pg.694]    [Pg.119]    [Pg.220]    [Pg.740]    [Pg.999]    [Pg.650]    [Pg.2245]    [Pg.651]    [Pg.13]    [Pg.13]    [Pg.24]   
See also in sourсe #XX -- [ Pg.580 ]




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Reserpinization

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