Parasympathetic nervous control of intraocular pressure

Electrical or chemical activation of the oculomotor nucleus (ONC) was performed in pentobarbital anesthetized cats to determine the role of parasympathetic nervous input to the eye in modulating intraocular pressure (IOP). In all animals, the vagosympathetic nerve trunks were sectioned bilaterally at the mid-cervical level. Intracranial stimulation of the ONC produced miosis and a bilateral sustained rise in IOP with little or no cardiovascular response. During stimulation, IOP increased by approximately 35-40%, with an additional small rise seen when the current was turned off. The secondary rise in IOP probably represents the actual pressure level reached which was otherwise masked by intense accommodation due to stimulation. The rise in IOP was not antagonized with gallamine triethiodide. However, both IOP and pupillary responses were blocked by either hexamethonium (1.5 mg kg-1, i.v.) or atropine (0.5 mg kg-1, i.v.). These results provide evidence for a neural parasympathetic mechanism for increasing IOP in cats. In another group, activation of ONC following electrolytic lesion of the preganglionic parasympathetic nerve to one eye, produced a rise in IOP and miosis only on the side with intact oculomotor nerve indicating that the rise in IOP is in part mediated by nerve fibers that travel to the eye along the oculomotor nerve trunk. Microinjection of L-glutamate (2.5 x 10(-7) M) into the ONC produced a bilateral rise in IOP that lasted for more than 15 min. This increase in IOP was greater than 50% of control levels and was accompanied with miosis.(ABSTRACT TRUNCATED AT 250 WORDS)