ArticlePediatric nephrology (Berlin, Germany)2006
Cyclosporin A stimulates apical Na+/H+ exchange in LLC-PK1/PKE20 proximal tubular cells.
Article in Pediatric nephrology (Berlin, Germany), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 6 citations in OpenAlex.
- Cyclosporine therapy in cytokine storm due to coronavirus disease 2019 (COVID-19).Rheumatology international · 2020Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cyclosporin A (CyA) causes renal Na(+) retention which may lead to arterial hypertension. The apical Na(+)/H(+) exchanger (NHE3) is responsible for bulk proximal tubular Na(+) reabsorption. The aim of this study was to investigate the effects of CyA on the NHE3 of polarized proximal tubular cells to evaluate cellular mechanisms of CyA-associated arterial hypertension. The change of the intracellular pH (Delta-[pH](i)/min) was determined as a measure of the activity of the NHE in LLC-PK(1)/PKE(20) cells using 2',7'-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein (BCECF). The NHE activity was identified as the apical NHE3 since it could be inhibited by the inhibitor S3226, but not by inhibitors of the basolateral isoform (NHE1) amiloride or HOE 694. CyA stimulated the NHE3 activity dose dependently. The mean increase stimulated by relevant CyA concentrations was 61+/-11%. A 24-h application of CyA also stimulated an increase of NHE3 activity which did not seem to be mediated by an increase of NHE3 RNA expression. The less immunosuppressive derivatives cyclosporin H and cyclosporin G caused NHE3 activation as well. Carbachol and ATP, which both induce a Ca(2+) release from internal Ca(2+) stores, also increased the NHE3 activity. The Ca(2+) chelator 1,2-bis-(2-aminophenoxy)-ethane-N,N,-N',N'-tetraacetic acid tetraacetoxymethyl ester (BAPTA-AM) abolished the CyA-associated NHE3 stimulation, whereas low extracellular Ca(2+) had no effect. CyA-associated effects did not seem to be mediated via inhibition of protein kinase C (PKC). CyA had no additive effects on the angiotensin II-associated NHE3 stimulation. Concurrent application of losartan did not impair the CyA-induced NHE3 stimulation. In conclusion CyA stimulates the apical NHE3 in proximal tubular cells. This is mediated by Ca(2+) release from intracellular stores but is independent of the action of angiotensin II or PKC.
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