May 1996
Volume 37, Issue 6
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Articles  |   May 1996
Beta-adrenergic stimulation of Na+, K+, Cl- cotransport in fetal nonpigmented ciliary epithelial cells.
Author Affiliations
  • R B Crook
    Department of Opthalmology, University of California, San Francisco 94143, USA.
  • K Riese
    Department of Opthalmology, University of California, San Francisco 94143, USA.
Investigative Ophthalmology & Visual Science May 1996, Vol.37, 1047-1057. doi:
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      R B Crook, K Riese; Beta-adrenergic stimulation of Na+, K+, Cl- cotransport in fetal nonpigmented ciliary epithelial cells.. Invest. Ophthalmol. Vis. Sci. 1996;37(6):1047-1057.

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Abstract

PURPOSE: The effects of adrenergic agonists and antagonists on Na+, K+, Cl- cotransport in fetal human nonpigmented ciliary epithelial (NPE) cells were investigated. METHODS: 86Rb+ as a marker for K+ was used to study ouabain-insensitive, bumetanide-sensitive 86Rb+ uptake in cultured NPE monolayers. Cyclic adenosine monophosphate (cAMP) formation in NPE cells was determined by radioimmunoassay. RESULTS: 1 microM isoproterenol caused a 1.65-fold stimulation in Na+,K+,Cl cotransport measured as bumetanide-sensitive, ouabain-insensitive 86Rb+ uptake. The half-maximal concentration for this effect was 6.4 nM, with maximal stimulation at 100 nM isoproterenol. Epinephrine stimulated Na+, K+, Cl- cotransport similarly to isoproterenol, whereas norepinephrine stimulated at much higher concentrations (half-maximal effective concentration = 1.4 microM). Stimulation of Na+, K+, Cl- cotransport by 1 microM isoproterenol was inhibited completely by the beta 2-adrenergic antagonist ICI-118,551 at 100 nM, with a half-maximal inhibitory concentration of 5 nM. Neither atenolol, a beta 1-specific adrenergic antagonist, prazosin, an alpha 1-adrenergic antagonist, nor yohimbine, an alpha 2-specific antagonist, was as effective. These four antagonists inhibited isoproterenol-stimulated cAMP formation with potencies similar to those observed against stimulated Na+, K+, Cl- cotransport. The hypotensive adrenergic antagonist timolol, propranolol, and betaxolol also inhibited Na+, K+, Cl- cotransport stimulated by isoproterenol in the order timolol > propranolol > betaxolol. Na+, K+, Cl- cotransport could be maintained in a stimulated state for at least 2 hours in the presence of agonist, but activity returned to basal levels within 20 minutes of isoproterenol removal. Adrenergic stimulation of Na+, K+, Cl- cotransport was blocked 80% to 85% by 70 microM H-89, a protein kinase A inhibitor. CONCLUSIONS: These data suggest that beta 2-adrenergic receptor activation results in increased cAMP formation and sustained stimulation of Na+, K+, Cl- cotransport in fetal human NPE cells. Protein kinase A activation is required for maximal stimulation of Na+, K+, Cl- cotransport by adrenergic agonists.

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