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Pilocarpine is a nonspecific muscarinic agonist commonly used to treat disorders of the eye. It reverses mydriasis, such as is caused by phenylephrine, and can be administered after an eye exam. Along with constricting the pupil through the smooth muscle of the iris, pilocarpine will also cause the ciliary muscle to contract. This will open perforations at the base of the cornea, allowing for the drainage of aqueous humor from the anterior compartment of the eye and, therefore, reducing intraocular pressure related to glaucoma.
Atropine and scopolamine are part of a class of muscarinic antagonists that come from the Atropa genus of plants that include belladonna or deadly nightshade ( [link] ). The name of one of these plants, belladonna, refers to the fact that extracts from this plant were used cosmetically for dilating the pupil. The active chemicals from this plant block the muscarinic receptors in the iris and allow the pupil to dilate, which is considered attractive because it makes the eyes appear larger. Humans are instinctively attracted to anything with larger eyes, which comes from the fact that the ratio of eye-to-head size is different in infants (or baby animals) and can elicit an emotional response. The cosmetic use of belladonna extract was essentially acting on this response. Atropine is no longer used in this cosmetic capacity for reasons related to the other name for the plant, which is deadly nightshade. Suppression of parasympathetic function, especially when it becomes systemic, can be fatal. Autonomic regulation is disrupted and anticholinergic symptoms develop. The berries of this plant are highly toxic, but can be mistaken for other berries. The antidote for atropine or scopolamine poisoning is pilocarpine.
| Sympathetic and Parasympathetic Effects of Different Drug Types | ||||
|---|---|---|---|---|
| Drug type | Example(s) | Sympathetic effect | Parasympathetic effect | Overall result |
| Nicotinic agonists | Nicotine | Mimic ACh at preganglionic synapses, causing activation of postganglionic fibers and the release of norepinephrine onto the target organ | Mimic ACh at preganglionic synapses, causing activation of postganglionic fibers and the release of ACh onto the target organ | Most conflicting signals cancel each other out, but cardiovascular system is susceptible to hypertension and arrhythmias |
| Sympathomimetic drugs | Phenylephrine | Bind to adrenergic receptors or mimics sympathetic action in some other way | No effect | Increase sympathetic tone |
| Sympatholytic drugs | β-blockers such as propanolol or metoprolol; α-agonists such as clonidine | Block binding to adrenergic drug or decrease adrenergic signals | No effect | Increase parasympathetic tone |
| Parasymphatho-mimetics/muscarinic agonists | Pilocarpine | No effect, except on sweat glands | Bind to muscarinic receptor, similar to ACh | Increase parasympathetic tone |
| Anticholinergics/muscarinic antagonists | Atropine, scopolamine, dimenhydrinate | No effect | Block muscarinic receptors and parasympathetic function | Increase sympathetic tone |
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