Rapid stimulation of Na+/H+ exchange by 1,25-dihydroxyvitamin D3; interaction with parathyroid-hormone-dependent inhibition |
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Authors: | Ulrich Binswanger Corinna Helmle-Kolb Judith Forgo Branka Mrkic Heini Murer |
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Institution: | (1) Department of Physiology, University of Zürich, Winterthurerstrasse 190, CH-8057 Zürich, Switzerland;(2) Department of Internal Medicine, University Hospital Zürich, Rämistrasse 100, CH-8091 Zürich, Switzerland |
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Abstract: | We have examined the rapid effect of 1,25-dihydroxyvitamin-D3 1,25(OH)2D3] on apical Na+/H+ exchange activity in opossum kidney (OK) cells and in MCT cells (a culture of simian-virus-40-immortalized mouse cortical tubule cells) grown on filter support. Addition of 1,25(OH)2D3 (10 nM) for 1 min increased apical Na+/H+ exchange activity recovery from an acid load; measured by 2 ,7 -bis(2-carboxyethyl)-5(6)-carboxyfluorescein] in OK cells (by 56%) and in MCT cells (by 36%). The cellular mechanisms involved in 1,25(OH)2D3-dependent stimulation of Na+/H+ exchange were analysed in OK cells; stimulation of Na+/ H+ exchange by 1,25(OH)2D3 was not prevented by actinomycin D. Applying parathyroid hormone (PTH) reduced Na+/H+ exchange activity in OK cells (by 34% at 10 nM, 5 min); 1,25(OH)2D3 reversed PTH-induced inhibition, either when PTH was added prior to 1,25(OH)2D3 or when the two agonists were applied together. 1,25(OH)2D3 had no effect on basal OK cell cAMP content or on Ca2+]i (fura-2). 1,25(OH)2D3 attenuated PTH-induced cAMP accumulation and had no effect on the PTH-dependent increase in Ca2+]i. These data suggest a regulatory control (stimulation) of proximal tubular brush-border Na+/H+ exchange by 1,25(OH)2D3. This effect is non-genomic and might in part be explained by a release from cAMP-dependent control of transport activity. |
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Keywords: | Na+/H+ exchange 1 25-dihydroxyvitamin D3 Parathyroid hormone |
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