Drugs that cause dilated pupil

[edit] Drugs
Anticholinergics such as atropine, hyoscyamine, and scopolamine antagonize the muscarinic acetylcholine receptors in the eye. By blocking these receptors, the pupils are no longer capable of constriction and dilation results. Such alkaloids present in many plants of the family Solanaceae may also induce mydriasis when used recreationally.[2]
Most hallucinogens such as LSD, psilocybin, and mescaline, in addition to some phenethylamines and tryptamines, all produce mydriasis by agonizing the serotonergic 5-HT2A receptors in the brain. Dissociatives such as ketamine, DXM, and PCP do so as well via antagonism of the NMDA glutamate receptors. There have also been reports that the atypical psychedelic herb salvia divinorum causes mydriasis. It works via agonism of the κ-Opioid receptors in the brain. How the neurological changes induced by these drugs ultimately causes pupil dilation is unknown.
Drugs that increase overall serotonin levels in general are capable of causing mydriasis in the same way as the 5-HT2A-mediated psychedelics. This is because serotonin itself is naturally responsible for normal 5-HT2A stimulation. Hence, in sufficient quantities serotonin is mydriatic and can even be mildly psychedelic, though the potentially fatal serotonin syndrome usually ensues before the psychedelia becomes overly-pronounced. Examples of such drugs include MDMA (as well as other MDxx compounds), fenfluramine, chlorphentermine, stimulants (including cocaine and amphetamines), and some antidepressants (such as SSRIs, SNRIs, and MAOIs). Natural serotonin-boosting supplements such as L-Tryptophan and 5-HTP are also capable of this, but usually only in excessive doses.
The neurotransmitter norepinephrine regulates many physiological processes in the body and brain. One of them is the autonomic constriction and contraction of certain muscles. The psychoactive drug cocaine potently inhibits the normal reuptake of norepinephrine into presynaptic nerve terminals resulting in an increased level of extracellular norepinephrine. Amphetamines also potently release and prevent the reuptake of norepinephrine. The released norepinephrine then proceeds to bind to adrenergic receptors, and the biological effects of norepinephrine finally occur. When a solution of cocaine is dropped into the eye, this process takes place, and the end result is dilation of the pupil. Cocaine itself is not typically used for this task however. Any potent norepinephrine reuptake inhibitor or release agent should be capable of such an effect.
Opioids such as morphine and heroin cause miosis. Subsequently, mydriasis occasionally occurs during opioid rebound and withdrawal.[3]