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Aqueous Humor Formation

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M. M. Civan – One of the best experts on this subject based on the ideXlab platform.

  • Basis of Chloride Transport in Ciliary Epithelium
    The Journal of Membrane Biology, 2004
    Co-Authors: C.w. Do, M. M. Civan

    Abstract:

    The Aqueous Humor is formed by the bilayered ciliary epithelium. The pigmented ciliary epithelium (PE) faces the stroma and the nonpigmented ciliary epithelium (NPE) contacts the Aqueous Humor. Cl^− secretion likely limits the rate of Aqueous Humor Formation. Many transport components underlying Cl^− secretion are known. Cl^− is taken up from the stroma into PE cells by electroneutral transporters, diffuses to the NPE cells through gap junctions and is released largely through Cl^− channels. Recent work suggests that significant Cl^− recycling occurs at both surfaces of the ciliary epithelium, providing the basis for modulation of net secretion. The PE-NPE cell couplet likely forms the fundamental unit of secretion; gap junctions within the PE and NPE cell layers are inadequate to maintain constancy of ionic composition throughout the epithelium under certain conditions. Although many hormones, drugs and signaling cascades are known to have effects, a persuasive model of the regulation of Aqueous Humor Formation has not yet been developed. cAMP likely plays a central role, potentially both enhancing and reducing secretion by actions at both surfaces of the ciliary epithelium. Among other hormone receptors, A_3 adenosine receptors likely alter intraocular pressure by regulating NPE-cell Cl^− channel activity. Recently, functional evidence for the regional variation in ciliary epithelial secretion has been demonstrated; the physiologic and pathophysiologic implications of this regional variation remain to be addressed.

  • Na^+/H^+ and Cl^–/HCO_3
    ^–-antiporters of bovine pigmented ciliary epithelial cells
    Pflügers Archiv, 2000
    Co-Authors: L. Counillon, Nicolas Touret, Michel Bidet, K. Peterson-yantorno, M. Coca-prados, Alan Stuart-tilley, Sabine Wilhelm, S.l. Alper, M. M. Civan

    Abstract:

    Medical therapy of glaucoma commonly aims at slowing Aqueous Humor Formation by the ocular ciliary epithelial bilayer, but underlying mechanisms are poorly understood. The first step in secretion is NaCl uptake from the stroma into the pigmented ciliary epithelial (PE) cell layer by electroneutral transporters. After crossing gap junctions into the nonpigmented ciliary epithelial (NPE) cell layer, solute is released into the Aqueous Humor. Published data have indicated that both paired Na^+/H^+ and Cl^–/HCO_3 ^– antiporters and the Na^+-K^+–2Cl^– symporter are involved in net uptake. The molecular identities of the paired antiporters have not been elucidated. We have studied continuously cultured bovine PE cells. Acid-activated ^22Na^+ uptake was inhibited by cariporide, EIPA (ethyl-isopropyl-amiloride) and amiloride, at concentrations characteristic of the NHE-1 isoform. Videomicroscopy of BCECF-loaded PE cells verified the presence of an EIPA-inhibitable Na^+/H^+ antiporter. Removing external Cl^– also triggered an alkalinization, which was Na^+-independent and could be inhibited by 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid (DIDS). Application of hypotonicity followed by return to isotonicity triggered a regulatory volume increase, which was pharmacologically similar to the uptake mechanisms described for intact rabbit ciliary epithelium. Reverse transcriptase polymerase chain reaction (RT-PCR) amplification of RNA from the human ciliary body detected expression of the AE2 Cl^–/HCO_3 ^– exchanger, but not of AE1, cAE3 or bAE3. Immunostaining of bovine PE cells also revealed the presence of AE2 epitope. We conclude that paired NHE-1 Na^+/H^+ and AE2 Cl^–/HCO_3 ^– antiporters are important components in the initial step in Aqueous Humor Formation.

  • Na+/H+ and Cl–/HCO3–-antiporters of bovine pigmented ciliary epithelial cells
    Pflügers Archiv – European Journal of Physiology, 2000
    Co-Authors: L. Counillon, Kim Peterson-yantorno, Nicolas Touret, Michel Bidet, M. Coca-prados, Alan Stuart-tilley, Sabine Wilhelm, S.l. Alper, M. M. Civan

    Abstract:

    Medical therapy of glaucoma commonly aims at slowing Aqueous Humor Formation by the ocular ciliary epithelial bilayer, but underlying mechanisms are poorly understood. The first step in secretion is NaCl uptake from the stroma into the pigmented ciliary epithelial (PE) cell layer by electroneutral transporters. After crossing gap junctions into the nonpigmented ciliary epithelial (NPE) cell layer, solute is released into the Aqueous Humor. Published data have indicated that both paired Na+/H+ and Cl–/HCO3 – antiporters and the Na+-K+–2Cl– symporter are involved in net uptake. The molecular identities of the paired antiporters have not been elucidated. We have studied continuously cultured bovine PE cells. Acid-activated 22Na+ uptake was inhibited by cariporide, EIPA (ethyl-isopropyl-amiloride) and amiloride, at concentrations characteristic of the NHE-1 isoform. Videomicroscopy of BCECF-loaded PE cells verified the presence of an EIPA-inhibitable Na+/H+ antiporter. Removing external Cl– also triggered an alkalinization, which was Na+-independent and could be inhibited by 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid (DIDS). Application of hypotonicity followed by return to isotonicity triggered a regulatory volume increase, which was pharmacologically similar to the uptake mechanisms described for intact rabbit ciliary epithelium. Reverse transcriptase polymerase chain reaction (RT-PCR) amplification of RNA from the human ciliary body detected expression of the AE2 Cl–/HCO3 – exchanger, but not of AE1, cAE3 or bAE3. Immunostaining of bovine PE cells also revealed the presence of AE2 epitope. We conclude that paired NHE-1 Na+/H+ and AE2 Cl–/HCO3 – antiporters are important components in the initial step in Aqueous Humor Formation.

Mortimer M. Civan – One of the best experts on this subject based on the ideXlab platform.

  • Pathways for ATP release by bovine ciliary epithelial cells, the initial step in purinergic regulation of Aqueous Humor inflow
    American Journal of Physiology-Cell Physiology, 2010
    Co-Authors: Chi Ting Leung, Kim Peterson-yantorno, Claire H. Mitchell, Mortimer M. Civan

    Abstract:

    ATP release by nonpigmented (NPE) and pigmented (PE) ciliary epithelial cells is the enabling step in purinergic regulation of Aqueous Humor Formation, but the release pathways are unknown. We meas…

  • Species variation in biology and physiology of the ciliary epithelium: similarities and differences.
    Experimental Eye Research, 2009
    Co-Authors: Mortimer M. Civan

    Abstract:

    � secretion HCO3 � secretion abstract Glaucoma is a leading cause of irreversible blindness worldwide. Lowering intraocular pressure (IOP) is the only strategy documented to delay the appearance and retard the progression of vision loss. One major approach for lowering IOP is to slow the rate of Aqueous Humor Formation by the ciliary epithe- lium. As discussed in the present review, the transport basis for this secretion is largely understood. However, several substantive issues are yet to be resolved, including the integrated regulation of secretion, the functional topography of the ciliary epithelium, and the degree and significance of species variation in Aqueous Humor inflow. This review discusses species differences in net secretion, particularly of Cl � and HCO3 secretion. Identifying animal models most accurately mimicking Aqueous Humor Formation in the human will facilitate development of future novel initiatives to lower IOP.

  • Mechanisms of Aqueous Humor Formation
    Ocular Transporters In Ophthalmic Diseases And Drug Delivery, 2008
    Co-Authors: Chi-wing Kong, Chu-yan Chan, Mortimer M. Civan

    Abstract:

    Glaucoma is a leading cause of irreversible blindness in the world (1). Primary openangle glaucoma (POAG) is the most common form of glaucoma and its onset, as well as progression, is often insidious, leading to significant visual loss before being clinically diagnosed. POAG is frequently associated with elevated intraocular pressure (IOP) of the eye. It is incurable at present, although its progression can be retarded by lowering the IOP by medication and/or surgery. If pharmacological agents fail to attain a targeted hypotensive response within the framework of the clinical characteristics and course, surgery will be indicated. The IOP is physiologically maintained within a relatively narrow range bracketing a mean of approximately 15 mmHg. The level of IOP reflects a dynamic balance between secretion (inflow) and drainage (outflow) of Aqueous Humor. The Aqueous Humor is a transparent fluid that is formed by the ciliary processes (epithelium) of the eye. After its production, Aqueous Humor flows from the posterior chamber to the anterior chamber of the eye via the pupil (Fig. 1). In the anterior chamber, the temperature difference between the warmer iris and the cooler cornea results in a convectional fluid circulation.

Maurizio Giacinto Uva – One of the best experts on this subject based on the ideXlab platform.

  • Pharmacological management of ocular hypertension: current approaches and future prospective
    Current Opinion in Pharmacology, 2012
    Co-Authors: Claudio Bucolo, Salvatore Salomone, Filippo Drago, Michele Reibaldi, Antonio Longo, Maurizio Giacinto Uva

    Abstract:

    Elevated eye pressure is the main risk factor for glaucoma, and intraocular pressure rises when the balance between Aqueous Humor Formation and outflow resistance is compromised. In a normal eye there is a precise tune of Aqueous outflow under the fine control of ciliary body and trabecular meshwork. Current pharmacological therapies for lowering the intraocular pressure in glaucoma include increasing Aqueous Humor outflow and suppression of Aqueous Humor production. However, most of antiglaucoma drugs currently on the market do not target the trabecular meshwork that represents the site of the pathology. This review focuses on pharmacological management of ocular hypertension with a particular attention to the future pharmacotherapy scenario.