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M M Civan

Publications and source records attributed to M M Civan.

112 records · Page 7Linked to original sources
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Formation of the aqueous humor.

1. Glaucoma is a worldwide disease affecting approximately 1-2% of the population aged over 35 years in industrial countries and is a major cause of blindness. 2. Glaucoma is usually associated with an increased intraocular pressure reflecting an imbalance between the rate of production of fluid (the aqueous humor) by the ciliary epithelial cells and its drainage from the eye. Therefore, it is important to understand how this secretion is produced. This requires a knowledge of ciliary epithelial cell composition, which has, in the past, proved difficult to obtain in mammalian preparations. 3. We have recently used the technique of electron-probe X-ray microanalysis to determine this composition under a variety of in vitro conditions. 4. Our results have led to a new model for this secretion that emphasizes the potential secretory role of the Na+/K+/2Cl- cotransporter.

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Swelling-activated chloride channels in aqueous humour formation: on the one side and the other.

Aqueous humour is secreted by the ciliary epithelium comprising pigmented and non-pigmented cell layers facing the stroma and aqueous humour respectively. Net chloride secretion likely limits the rate of aqueous humour formation and proceeds in three steps: stromal chloride entry into pigmented cells, diffusion through gap junctions and final non-pigmented cell secretion. Swelling-activated chloride channels function on both epithelial surfaces. At the stromal surface, swelling- and cyclic adenosine monophosphate-activated maxi-chloride channels can recycle chloride, reducing net chloride secretion. At the aqueous-humour surface, swelling- and A3 adenosine receptor-activated chloride channels subserve chloride release into the aqueous humour. The similar macroscopic properties of the two non-pigmented cell chloride currents suggest that both flow through a common conduit. In addition, measurements of intraocular pressure (IOP) in living wild-type and mutant mice have confirmed that A3 adenosine receptor-activated agonists and antagonists increase and lower IOP respectively. Isolated ciliary epithelial cells are commonly perfused with hypotonic solution to probe and characterize chloride channels, but the physiological role of swelling-activated channels has been unclear without knowing their epithelial distribution. Recently, hypotonic challenge has been found to stimulate the chloride-sensitive short-circuit current across the intact bovine ciliary epithelium, suggesting that the net effect of the swelling-activated chloride currents is oriented to enhance aqueous humour formation. Taken together, the results suggest that swelling-activated chloride channels are predominantly oriented to enhance aqueous humour secretion, and these chloride channels at the aqueous surface may be identical with adenosine receptor-activated chloride channels which likely modulate aqueous inflow and IOP in the living mouse.

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