Depleting agent

Neuronal norepinephrin depleting agents [50-55-5] C2 H4QN20g Serpasil, Reserpoid... 

Neuronal Norepinephrine Depleting Agents. Reserpine (Table 6) is the most active alkaloid derived from Rauwolfia serpentina. The principal antihypertensive mechanism of action primarily results from depletion of norepinephrine from peripheral sympathetic nerves and the brain adrenergic neurons. The result is a drastic decrease in the amount of norepinephrine released from these neurons, leading to decrease in vascular tone and lowering of blood pressure. Reserpine also depletes other transmitters including epinephrine, serotonin [50-67-9] dopamine [51-61-6] ... 

MTX caused a contraction of vascular smooth muscle and positive inotropic, positive chronotropic and arrhythmogenic effects on cardiac muscle. The effect of MTX was little affected by various receptor blockers, a Na channel blocker or a catecholamine depleting agent. Further, MTX had no effect on the enzymes which were related to Ca movements, such as Na , K -ATPase, cyclic AMP phosphodiesterase, and sarcoplasmic reticulum Ca -ATPase. These results would eliminate the possible involvement of an indirect action elicited by the release of chemical mediators and direct modifications of their receptors, Na channels, or various enzymes as a major mechanism of action of MTX. 

Nitrous oxide has received increasing attention the last decade, due to the growing awareness of its impact on the environment, as it has been identified as an ozone depletion agent and as a Greenhouse gas [1]. Identified major sources include adipic acid production, nitric acid and fertilizer plants, fossil fuel and biomass combustion and de-NOx treatment techniques, like three-way catalysis and selective catalytic reduction [2,3]. 

Comporti, M. (1987). Glutathione depleting agents and lipid peroxidation. Chem. Phys. Lipids 45, 143-169. 

Symptomatic treatment. The chorea of Huntington s disease responds (partially) to treatment with neuroleptics, which, through blockade of D2 receptors, may help to increase basal ganglia output to more normal levels. Dopamine-depleting agents, such as reserpine or tetra-benazine have also been used. At best, these agents are only moderately effective and they should only be used if the chorea truly interferes with activities of daily living or produces social embarrassment. Neuroleptics and... 

Dopamine depleting agents. Reserpine, a natural alkaloid that blocks vesicular transport of monoamines, depletes stored monoamines, including DA. DA depletion is associated with the emergence of parkinsonism. This effect of reserpine was among the first clues that PD is the result of DA deficiency (see above). Generally, the parkinsonism resulting from reserpine is reversible. 

Drugs that may be affected by carvedilol include antidiabetic agents, calcium blockers, clonidine, cyclosporine, disopyramide, catecholamine depleting agents (eg, reserpine), and digoxin. 

The effect of glutathione-depleting agents on the amounts of cellular chromium(in) and chromium(V) was determined in Chinese hamster V-79 cells treated with sodium chromate (Sugiyama and Tsuzuki 1994). Buthionine sulfoximine at 25 pM reduced glutatione levels to about 1% of control values, and increased chromium(V) levels by about 67%. The total chromium uptake was decreased by about 20%, and chromium(III) levels were decreased by 20%. Diethylmaleate (1 mM) decreased glutathione levels less than 1%, decreased chromium(V) levels by 27%, and chromium(in) levels by 31%. However, the... 

Langley-Evans, S.C., G.J.Phillips, and A.A.Jackson. 1996. Sulfur dioxide A potent glutathione depleting agent. Comp. Biochem. Physiol. C Pharmacol. Toxicol. Endocrinol. 114(2) 89—... 

As in AD, knowdedge of the neurotransmitter deficiency underlying PD, in this case dopamine, has been the basis for the development of therapy. Early studies show ed that cerebral dopamine was concentrated in the shiatum and that levodopa, the precursor to dopamine, could reverse the akinetic effects of the dopamine-depleting agent reserpine in experimental animals (Carlsson et al., 1957, 1958). Eventually, the identification of shiatal dopamine depletion as a key neurochemical finding in parkinsonian brains lead to heatment wdth levodopa in humans and to the subsequent advent of compounds that mimic the effects of dopamine or prolong its action (Table 39.2). 

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