Nicotine is a central nervous system stimulant that affects various bodily functions, including heart rate and blood pressure. While many psychoactive substances have a clear effect on pupil size, nicotine’s physiological response is more complex. Studies often observe a slight, acute constriction in many cases, a paradoxical effect rooted in the drug’s powerful and nonselective interaction with the body’s involuntary control system, the autonomic nervous system.
Nicotine and the Autonomic Nervous System
Nicotine acts as a nonselective cholinergic nicotinic agonist, mimicking the neurotransmitter acetylcholine. It binds to and activates nicotinic acetylcholine receptors (nAChRs) throughout the central and peripheral nervous systems. These receptors are widely distributed at junctions where nerve signals relay throughout the body.
The autonomic nervous system (ANS) is divided into the Sympathetic Nervous System (SNS) for “fight or flight,” and the Parasympathetic Nervous System (PNS) for “rest and digest.” Nicotine activates the ganglia, which are relay centers for both the SNS and the PNS. This simultaneous stimulation of opposing systems makes nicotine’s net effect on any single organ, including the eye, difficult to predict. While nicotine often causes systemic sympathetic activation, the specific pathways controlling the pupil are highly sensitive.
The Body’s Regulation of Pupil Size
The pupil’s diameter is regulated by two opposing muscles within the iris, ensuring the correct amount of light reaches the retina. This reflex mechanism is controlled by the autonomic nervous system. The sphincter pupillae muscle encircles the pupil and is responsible for constriction (miosis), managed by the parasympathetic system.
The dilator pupillae muscle is arranged radially and is responsible for widening the pupil (mydriasis), controlled by the sympathetic nervous system. Pupil size is a balance between these two muscle groups, which continuously receive opposing instructions from the SNS and the PNS. Any drug that interferes with the signals to these muscles can alter the pupil’s diameter.
The Actual Effect of Nicotine on Pupils
The most commonly observed acute effect of nicotine intake on the pupil is constriction, or miosis. Studies involving both smokers and non-smokers, using nicotine gum or a single cigarette, frequently record a measurable decrease in pupil size shortly after administration. This suggests that, despite the widespread sympathetic activation seen in the cardiovascular system, the parasympathetic control over the sphincter pupillae muscle appears relatively more dominant in the acute phase of nicotine exposure.
This acute constriction is a surprising finding, as sympathetic activation is typically associated with dilation. It highlights the nonselective nature of nicotine, where the transient dominance of the parasympathetic pathway on the iris muscles overrides the expected sympathetic-driven dilation. However, the long-term or chronic effects of nicotine can be different, with some data suggesting chronic use may lead to a slight enlargement of the pupil.
The ultimate effect of nicotine on pupil size is highly dependent on factors such as the dose administered, the user’s history, and the specific conditions of measurement. The temporary constriction observed is a localized outcome of complex, systemic stimulation of both the sympathetic and parasympathetic branches of the autonomic nervous system. This nuanced response contrasts with drugs like opioids, which cause uniform constriction, or stimulants like cocaine, which cause uniform dilation.