ABSTRACT
Hepatic esterase and nonhepatic cytochrome P-450 play minor roles in cocaine metabolism. Increased or decreased central nervous system outflow determines how much neurotransmitter is actively released from distal nerve terminals, and thus influences cocaine's effect. Perfused hearts from both groups showed similar responses to cocaine, and there were no differences in resting autonomic tone or cocaine metabolism between the two groups. While the central nervous system may mediate some of cocaine's effects, its precise role remains unclear. Cocaine's effect on placental and endothelialprostaglandin production could explain the inability of alpha receptor antagonists to completely block cocaine's vasoconstrictive effect. In rat liver cell cultures, hepatic demethylation accounts for approximately 20% of cocaine's metabolism. The myometrium is sensitive to adrenergic stimulation, and because cocaine prolongs the stimulatory effect of catecholamines on adrenergic receptors, cocaine's relation to uterine contractility has been studied.
