At this point, neural activity decreases greatly; the continual blockade of receptors only compounds this effect.Chlorpromazine acts as an antagonist (blocking agent) on different postsynaptic and presynaptic receptors:

Dopamine receptors (subtypes D1, D2, D3 and D4), which account for its different antipsychotic properties on productive and unproductive symptoms, in the mesolimbic dopamine system accounts for the antipsychotic effect whereas the blockade in the nigrostriatal system produces the extrapyramidal effects
Serotonin receptors (5-HT2, 5-HT6 and 5-HT7), with anxiolytic, antidepressant and antiaggressive properties as well as an attenuation of extrapyramidal side effects, but also leading to weight gain and ejaculation difficulties. Histamine receptors (H1 receptors, accounting for sedation, antiemetic effect, vertigo, and weight gain)
α1- and α2-adrenergic receptors (accounting for sympatholytic properties, lowering of blood pressure, reflex tachycardia, vertigo, sedation, hypersalivation and incontinence as well as sexual dysfunction, but may also attenuate pseudoparkinsonism – controversial. Also associated with weight gain as a result of blockage of the adrenergic alpha 1 receptor)
M1 and M2 muscarinic acetylcholine receptors (causing anticholinergic symptoms such as dry mouth, blurred vision, constipation, difficulty or inability to urinate, sinus tachycardia, electrocardiographic changes and loss of memory, but the anticholinergic action may attenuate extrapyramidal side effects).The presumed effectiveness of the antipsychotic drugs relied on their ability to block dopamine receptors. This assumption arose from the dopamine hypothesis that maintains that both schizophrenia and bipolar disorder are a result of excessive dopamine activity. Furthermore, psychomotor stimulants like cocaine that increase dopamine levels can cause psychotic symptoms if taken in excess.Chlorpromazine and other typical antipsychotics are primarily blockers of D2 receptors.
Sodium calcium edetate (sodium calcium EDTA), also known as edetate calcium disodium among other names, is a medication primarily used to treat lead poisoning, including both short-term and long-term lead poisoning. Sodium calcium edetate came into medical use in the United States in 1953. Chelation agent
Sodium calcium edetate is in the chelating agent family of medication. It is a salt of edetate with two sodium and one calcium atoms. It works by binding to a number of heavy metals, which renders them almost inert and allows them to leave the body in the urine.Edetate disodium is a different formulation which does not have the same effects. Medical use
Sodium calcium edetates primary use is to treat lead poisoning,
for which it is an alternative to succimer. It is given by slow injection into a vein or into a muscle.For lead encephalopathy sodium calcium edetate is typically used together with dimercaprol. It may also be used to treat plutonium poisoning. It does not appear to be useful for poisoning by tetra-ethyl lead. Side effects
Common side effects include pain at the site of injection. Other side effects may include kidney problems, diarrhea, fever, muscle pains, and low blood pressure. Benefits when needed in pregnancy are likely greater than the risks. History
Sodium calcium edetate came into medical use in the United States in 1953. It is on the World Health Organizations List of Essential Medicines. References
External links
"Sodium calcium edetate". U.S. National Library of Medicine. Drug Information Portal. U.S. National Institutes of Health.