NDLI: Electron probe X-ray microanalysis of intact pathway for human aqueous humor outflow

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	McLaughlin, Charles W. Karl, Mike O. Zellhuber-McMillan, Sylvia Wang, Zhao Do, Chi Wai Leung, Chi Ting Li, Ang Stone, Richard A. Macknight, Anthony D. C. Civan, Mortimer M.
Description	Country affiliation: New Zealand Author Affiliation: McLaughlin CW ( Dept. of Physiology, University of Otago Medical School, Dunedin, New Zealand.)
Abstract	Intraocular pressure (IOP) is regulated by the resistance to outflow of the eye's aqueous humor. Elevated resistance raises IOP and can cause glaucoma. Despite the importance of outflow resistance, its site and regulation are unclear. The small size, complex geometry, and relative inaccessibility of the outflow pathway have limited study to whole animal, whole eye, or anterior-segment preparations, or isolated cells. We now report measuring elemental contents of the heterogeneous cell types within the intact human trabecular outflow pathway using electron-probe X-ray microanalysis. Baseline contents of Na(+), K(+), Cl(-), and P and volume (monitored as Na+K contents) were comparable to those of epithelial cells previously studied. Elemental contents and volume were altered by ouabain to block Na(+)-K(+)-activated ATPase and by hypotonicity to trigger a regulatory volume decrease (RVD). Previous results with isolated trabecular meshwork (TM) cells had disagreed whether TM cells express an RVD. In the intact tissue, we found that all cells, including TM cells, displayed a regulatory solute release consistent with an RVD. Selective agonists of A(1) and A(2) adenosine receptors (ARs), which exert opposite effects on IOP, produced similar effects on juxtacanalicular (JCT) cells, previously inaccessible to functional study, but not on Schlemm's canal cells that adjoin the JCT. The results obtained with hypotonicity and AR agonists indicate the potential of this approach to dissect physiological mechanisms in an area that is extremely difficult to study functionally and demonstrate the utility of electron microprobe analysis in studying the cellular physiology of the human trabecular outflow pathway in situ.
File Format	HTM / HTML
ISSN	03636143
e-ISSN	15221563
DOI	10.1152/ajpcell.340.2008
Journal	American Journal of Physiology - Cell Physiology
Issue Number	5
Volume Number	295
Language	English
Publisher	American Physiological Society
Publisher Date	2008-11-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Cell Biology Aqueous Humor Metabolism Electron Probe Microanalysis Trabecular Meshwork Adenosine Analogs & Derivatives Pharmacology Adenosine A1 Receptor Agonists Adenosine A2 Receptor Agonists Cell Size Chlorides Enzyme Inhibitors Feasibility Studies Hypotonic Solutions Intraocular Pressure Norbornanes Osmotic Pressure Ouabain Phenethylamines Phosphorus Potassium Receptor, Adenosine A1 Receptors, Adenosine A2 Sodium Sodium-potassium-exchanging Atpase Antagonists & Inhibitors Cytology Drug Effects Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Cell Biology Physiology

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