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Muscarinic Receptor Agonists and Antagonists: Effects on Ocular Function

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Part of the book series: Handbook of Experimental Pharmacology ((HEP,volume 208))

Abstract

Muscarinic agonists act mainly via muscarinic M3 cholinoceptors to cause contraction of the iris sphincter, ciliary muscle and trabecular meshwork as well as increase outflow facility of aqueous humour. In the iris dilator, the effect of muscarinic agonists is species dependent but is predominantly relaxation via muscarinic M3 receptors. In the conjunctiva, muscarinic agonists stimulate goblet cell secretion which contributes to the protective tear film. Muscarinic M2 and M3 receptors appear mainly involved. In the lens muscarinic agonists act via muscarinic M1 receptors to produce depolarization and increase [Ca2+]i. All five subtypes of muscarinic receptor are present in the retina. In the developing retina, acetylcholine appears to limit purinergic stimulation of retinal development and decrease cell proliferation. In the adult retina acetylcholine and other muscarinic agonists may have complex effects, for example, enhancing light-evoked neuronal firing in transient ON retinal ganglion cells and inhibiting firing in OFF retinal ganglion cells. In the lacrimal gland, muscarinic agonists activate M3 receptors on secretory globular acinar cells to stimulate tear secretion and also cause contraction of myoepithelial cells. In Sjögren’s syndrome, antibodies to the muscarinic M3 receptor disrupt normal gland function leading to xerophthalmia although the mechanism of action of the antibody is still not clear. Atropine and pirenzepine are useful in limiting the development of myopia in children probably by an action on muscarinic receptors in the sclera, although many other muscarinic receptor antagonists are not effective.

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Mitchelson, F. (2012). Muscarinic Receptor Agonists and Antagonists: Effects on Ocular Function. In: Fryer, A., Christopoulos, A., Nathanson, N. (eds) Muscarinic Receptors. Handbook of Experimental Pharmacology, vol 208. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-23274-9_12

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