ArticlePflugers Archiv : European journal of physiology1993
Rapid stimulation of Na+/H+ exchange by 1,25-dihydroxyvitamin D3; interaction with parathyroid-hormone-dependent inhibition.
Article in Pflugers Archiv : European journal of physiology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 16 citations in OpenAlex.
- Fructose-Rich Diet Is a Risk Factor for Metabolic Syndrome, Proximal Tubule Injury and Urolithiasis in Rats.International journal of molecular sciences · 2021Article
- Proximal tubular NHEs: sodium, protons and calcium?American journal of physiology. Renal physiology · 2013Review
- The epithelial sodium/proton exchanger, NHE3, is necessary for renal and intestinal calcium (re)absorption.American journal of physiology. Renal physiology · 2012Article
- Regulation of rat ileal NHE3 by 1,25(OH)2-vitamin D3.Digestive diseases and sciences · 2002Article
- Stimulation of Na+/H+ exchange activity by endothelin in opossum kidney cells.Pflugers Archiv : European journal of physiology · 1995Article
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Authors and funding
5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
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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