Читать книгу Essentials of Veterinary Ophthalmology - Kirk N. Gelatt - Страница 96

Cholinergic agonists such as pilocarpine decrease outflow resistance by contraction of the ciliary muscle and subsequent spreading of the TM. This effect is rapid, such that intravenous administration of pilocarpine to vervet monkeys results in a near‐instantaneous decrease in outflow resistance, suggesting that the effect may be mediated by a structure perfused by arteries. Ciliary muscle disinsertion and removal of the iris in nonhuman primates obliterate this acute response to pilocarpine, suggesting that it is mediated completely by ciliary muscle contraction rather than a direct effect on the TM. The M3 subtype of the muscarinic receptor is strongly expressed in the ciliary muscle and thought to mediate the changes in outflow facility in response to cholinergic agonists. Because the effect of cholinergic agonists on trabecular outflow (increase) is greater than that on uveoscleral outflow (decrease), the net effect is an increase in AH outflow and concomitant decrease in IOP. As expected, cholinergic antagonists, such as atropine, decrease traditional outflow and increase nontraditional outflow by similar mechanisms.

Many other influences on the rate of AH formation and regulation of IOP have been proposed. For example, a center in the feline diencephalon has been found that, when stimulated, causes alterations in the IOP. Central nervous system (CNS) regulation of IOP is poorly understood, however, and hormonal control of AH production may be involved.