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Mansim C. Okafor, Nicholas A. Delamere; The Inhibitory Influence of Endothelin on Active Sodium-Potassium Transport in Porcine Lens. Invest. Ophthalmol. Vis. Sci. 2001;42(5):1018-1023.
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purpose. Endothelin (ET)-1 is known to inhibit active NaK transport by as much
as 50% in kidney tubule and other tissues. The presence of low levels
of ET-1 in aqueous humor combined with the potential for release of
ET-1 from ciliary processes suggests that the lens could be exposed to
ET-1 in vivo. In this study, experiments were conducted to examine the
influence of ET-1 on active NaK transport in porcine lens.
methods. The rate of Na,K-adenosine triphosphatase (Na,K-ATPase) dependent
potassium transport was determined by measurements of ouabain-sensitive
potassium (86Rb) uptake by intact lenses. Lens sodium
content was measured by atomic absorption spectrophotometry. Cyclic
adenosine monophosphate (cAMP) was measured by radioimmunoassay.
Cytoplasmic calcium concentration in cultured porcine lens epithelium
was measured by a fluorescence technique using fura-2.
results. In the presence of ET-1 (0.1 nM or higher concentration), the rate of
ouabain-sensitive potassium (86Rb) uptake was diminished.
The ET receptor antagonist PD145065 (2 μM) suppressed the inhibitory
effect of ET-1 (100 nM) on 86Rb uptake. Sodium content was
detectably increased in lenses exposed to ET-1 for 24 hours. Forskolin
(1 μM) caused an eightfold increase of cAMP in the lens epithelium,
but no increase of cAMP was detected in the epithelium of lenses
treated with ET-1. Genistein (150 μM), an inhibitor of tyrosine
kinases, abolished the inhibitory effects of ET-1 on lens 86Rb uptake. ET-1 caused an increase of cytoplasmic calcium
concentration in cultured porcine lens epithelium. The cytoplasmic
calcium response to ET-1 was inhibited by PD145065 and genistein.
conclusions. The results of the present study suggest that ET-1 causes inhibition of
lens active Na-K transport by a mechanism that involves activation of
ET receptors. Activation of ET receptors also causes an increase of
cytoplasmic calcium concentration in cultured lens epithelial cells.
Both responses to ET-1 appear to have a tyrosine kinase step, because
they could be prevented by genistein. The physiological purpose of an
ET-1–induced reduction in the rate of active Na-K transport by the
lens is unknown at this time.
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