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Investigative Ophthalmology & Visual Science, Vol 32, 3033-3040, Copyright © 1991 by Association for Research in Vision and Ophthalmology
ARTICLES AND REPORTS |
JL Edelman and SS Miller
University of California, School of Optometry, Berkeley 94720.
The authors used a modified capacitive probe technique to simultaneously assess the effect of apical epinephrine on fluid transport rate (Jv), transepithelial potential (TEP), and transepithelial resistance (Rt) across bovine retinal pigment epithelium (RPE). In control Ringer, the RPE absorbed fluid at a rate of 1.42 +/- 0.34 microliters/cm2.hr (mean +/- SEM; 22 tissues). Tissues with the highest TEP (8-9 mV) and Rt (160-220 omega.cm2) had maximum fluid absorption rates (3-4 microliters/cm2.hr). Apical epinephrine (100 nM) stimulated Jv by a factor of 3, from 0.70 +/- 0.18 microliter/cm2.hr to 2.17 +/- 0.24 microliters/cm2.hr and TEP from 4.6 +/- 0.4 mV to 7.0 +/- 0.6 mV (n = 6). The epinephrine-induced transport changes were inhibited by apical bumetanide (0.1 mM). The alpha-1 adrenergic antagonist prazosin (1 microM) completely blocked the epinephrine-induced stimulation of Jv and TEP. In contrast, the beta adrenergic antagonist propranolol (1 microM) had no effect on epinephrine-induced transport changes. These results, coupled with previous studies on bovine RPE, suggest that the mechanisms underlying the epinephrine-induced stimulation of fluid absorption include an apical membrane alpha-1 adrenergic receptor, a bumetanide-inhibitable apical membrane Na-K-2Cl cotransporter, and a basolateral membrane Cl conductance.
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