1Toxin of puffer fish, California newt. 2Toxin of Gonyaulax (red tide organism). 3Norepinephrine, dopamine, acetylcholine, angiotensin II, various prostaglandins, etc. 4Toxin of marine snails of the genus Conus. 5Black widow spider venom. 6Serotonin, norepinephrine reuptake inhibitors. NET, norepinephrine transporter; SNRI, serotonin-norepinephrine reuptake inhibitors; VAT, vesicle-associated transporter; VMAT, vesicular monoamine transporter.
The eye is a good example of an organ with multiple auto-nomic functions, controlled by several autonomic receptors. As shown in Figure 6–9, the anterior chamber is the site of several autonomic effector tissues. These tissues include three muscles (pupillary dilator and constrictor muscles in the iris and the ciliary muscle) and the secretory epithelium of the ciliary body. Parasympathetic nerve activity and muscarinic cholinomi-metics mediate contraction of the circular pupillary constrictor muscle and of the ciliary muscle. Contraction of the pupillary constrictor muscle causes miosis, a reduction in pupil size. Miosis is usually present in patients exposed to large systemic or small topical doses of cholinomimetics, especially organophosphate cholinesterase inhibitors. Ciliary muscle contraction causes accom-modation of focus for near vision. Marked contraction of the ciliary muscle, which often occurs with cholinesterase inhibitor intoxication, is called cyclospasm. Ciliary muscle contraction also puts tension on the trabecular meshwork, opening its pores and facilitating outflow of the aqueous humor into the canal of Schlemm. Increased outflow reduces intraocular pressure, a very useful result in patients with glaucoma. All of these effects are pre-vented or reversed by muscarinic blocking drugs such as atropine. Alpha adrenoceptors mediate contraction of the radially oriented pupillary dilator muscle fibers in the iris and result in mydriasis. This occurs during sympathetic discharge and when α-agonist drugs such as phenylephrine are placed in the conjunctival sac. Beta adrenoceptors on the ciliary epithelium facilitate the secretion of aqueous humor. Blocking these recep-tors (with β-blocking drugs) reduces the secretory activity and reduces intraocular pressure, providing another therapy for glaucoma.
currently available drugs: adrenoceptors are easily distinguished from cholinoceptors. Furthermore, individual receptor subgroups can often be selectively activated or blocked within each major type. Some examples are given in the Box: Pharmacology of the Eye. Even greater selectivity may be attainable in the future using drugs that target post-receptor processes, eg, receptors for second messengers. The next four chapters provide many more examples of this useful diversity of autonomic control processes.
FIGURE 6–9 Structures of the anterior chamber of the eye. Tissues with significant autonomic functions and the associated ANS receptors (α, β, M) are shown in this schematic diagram. Aqueous humor is secreted by the epithelium of the ciliary body, flows into the space in front of the iris, flows through the trabecular meshwork, and exits via the canal of Schlemm (arrow). Blockade of the β adrenoceptors associated with the ciliary epithelium causes decreased secretion of aqueous. Blood vessels (not shown) in the sclera are also under autonomic control and influence aqueous drainage.
Andersson K-E: Mechanisms of penile erection and basis for pharmacological treatment of erectile dysfunction. Pharmacol Rev 2011;63:811.