Journal
JOURNAL OF GENERAL PHYSIOLOGY
Volume 119, Issue 6, Pages 561-569Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1085/jgp.20028597
Keywords
water transport; AQP1; AQP4; anterior chamber; transgenic mice
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Funding
- NEI NIH HHS [EY 13574, R01 EY013574] Funding Source: Medline
- NHLBI NIH HHS [R01 HL059198, HL 59198, HL 60288] Funding Source: Medline
- NIBIB NIH HHS [R01 EB000415, R37 EB000415, EB 40015] Funding Source: Medline
- NIDDK NIH HHS [DK 35124, R01 DK035124, R37 DK035124] Funding Source: Medline
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Aquaporin (AQP) water channels are expressed in the eye at sites of aqueous fluid production and outflow: AQP1 and AQP4 in nonpigmented ciliary epithelium, and AQP1 in trabecular meshwork endothelium. Novel methods were developed to compare aqueous fluid dynamics in wild-type mice versus mice lacking AQP1 and/or AQP4. Aqueous fluid production Was measured by in vivo confocal microscopy after transcorneal iontophoretic introduction of fluorescein. Intraocular pressure (IOP), outflow, and anterior chamber compliance were determined from pressure measurements in response to fluid infusions using micropipettes. Aqueous fluid volume and [Cl-] were assayed in samples withdrawn by micropipettes. In wild-type mice (CD1 genetic background, age 4-6 wk), IOP was 16.0 +/- 0.4 mmHg (SE), aqueous fluid volume 7.2 +/- 0.3 mul, fluid production 3.6 +/- 0.2 mul/h, fluid outflow 0.36 +/- 0.06 mul/h/mmHg, and compliance 0.036 +/- 0.006 mul/mmHg. IOP was significantly decreased by up to 1.8 mmHg (P < 0.002) and fluid production by up to 0.9 mul/h in age/litter-matched mice lacking AQP1 and/or AQP4 (outbred CD1 and inbred C57/b16 genetic backgrounds). However, AQP deletion did not significantly affect outflow, [Cl-], volume, or compliance. These results provide evidence for the involvement of AQPs in intraocular pressure regulation by facilitating aqueous fluid secretion across the ciliary epithelium. AQP inhibition may thus provide a novel approach for the treatment of elevated IOP.
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