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Jodi Rymer, Sheldon S. Miller, Jeffrey L. Edelman; Epinephrine-Induced Increases in [Ca2+]in and KCl-Coupled Fluid Absorption in Bovine RPE. Invest. Ophthalmol. Vis. Sci. 2001;42(8):1921-1929. doi: https://doi.org/.
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© ARVO (1962-2015); The Authors (2016-present)
purpose. To define the ionic basis for the apical epinephrine-induced increase
of fluid absorption (J V) across isolated
methods. Epinephrine-induced changes in RPE [Ca2+]in levels were monitored with the ratioing dye fura-2. Transepithelial
potential, resistance, and unidirectional fluxes of 36Cl, 86Rb (K substitute), and 22Na were
simultaneously determined in paired tissues from the same eye mounted
in modified Üssing flux chambers. Radioisotopes (5–7 μCi) were
added to the apical bath of one tissue and the basal bath of the other,
and the appearance of label in the opposite bath was measured.
results. Apical epinephrine (100 nM) transiently increased[
Ca2+]in by 153 ± 78 nM. This increase
was inhibited by the α1-adrenoreceptor antagonist
prazosin (1 μM) and blocked by CPA(5 μM), an inhibitor of
endoplasmic reticulum Ca2+-adenosine triphosphatases
(ATPases). Apical epinephrine (100 nM) more than doubled the net Cl
absorption rate, increased net K (86Rb) absorption by
fivefold, and tripled net fluid absorption
(J V), as predicted by isotonic
coupling between ion and fluid transport. The epinephrine-induced
increases in ion and fluid transport were completely inhibited by
apical bumetanide (100 μM).
conclusions. Epinephrine increased fluid absorption across bovine RPE by activating
apical membrane α1-adrenergic receptors, increasing[
Ca2+]in, and stimulating
bumetanide-sensitive Na,K,2Cl uptake at the apical membrane and KCl
efflux at the basolateral membrane.
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