Regulation of Intraocular Pressure after Water Drinking

Abstract

Acute oral water loading transiently elevates intraocular pressure (IOP) via mechanisms that remain unexplained. We tested the possibilities that water drinking might elevate IOP by creating a blood-aqueous osmotic gradient, or that it might instead alter active ion pumping and the formation of aqueous humor. In the first series, 16 young, healthy individuals were studied during dehydration and for 1 hour after rehydration (14 mL H2O/kg body weight). Hematocrit, total plasma osmolality, and plasma colloid osmotic pressure were determined simultaneously with measurements of IOP. In a second series (N = 16), rehydration occurred after pretreatment with either placebo or a topical carbonic anhydrase inhibitor (1 drop 2% dorzolamide in each eye, 12 and 2 hours before oral water loading). In both series, mean IOP increased significantly 15 minutes after water ingestion and remained elevated above baseline for 45 minutes. In contrast, colloid osmotic pressure and hematocrit were unaltered by water drinking, and neither these variables nor total plasma osmolality correlated with IOP. In the second series, pretreatment with dorzolamide reduced baseline IOP, but failed to alter the magnitude or time course of IOP elevations induced by water drinking. Because water drinking failed to create a blood-ocular osmotic pressure gradient, neither vitreous hydration nor increased aqueous ultrafiltration can explain increases in IOP after acute hydration. Because the increase in ocular tension apparently also is independent of active bicarbonate pumping, factors affecting aqueous drainage must explain the water drinking effect.