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Figure 1 .

A corneal endothelial cell with receptors to adenosine, acetylcholine, and platelet activating factor, and the cell signalling cascades that would presumably follow the binding of such compounds. The cell would be polarised, with the transporters and/or channels involved in regulatory volume increase (RVI) located in the basolateral membrane, and those for regulatory volume decrease (RVD) in the apical membrane. These two sets of transporters/channels would be activated each by a different signalling cascade; one possible arrangement is shown, with protein kinase A triggering RVI and protein kinase C triggering RVD. AQP = aquaporins.
Figure 2 .
A model for fluid transport across corneal endothelium. Water passage is shown across aquaporins or water channels. The distribution indicated for the membrane proteins is assumed, except for the Na+ pump (long known to be basolateral) and the aquaporins, since our own evidence (J Li, K Kuang, S Nielsen, J Fischbarg, in preparation) places them in both apical and basolateral membranes. With the cell polarised as shown, fluid transport from stroma to aqueous could result from successive volume increase-decrease cycles analogous to those in RVI and RVD. PAF = platelet activating factor.
Figure 3 .
Schematic depiction of the temporal events postulated for a cycle of pulsatile endothelial fluid transport. Transient local osmotic gradients are denoted by the shading indicating osmolyte buildup on one side of the membrane (the concomitant depletion on the other side of the membrane is omitted). Osmolyte flux, solid arrows; water flow, broken arrows.
Selected References
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