ArticleThe Journal of membrane biology1997
Cross talk of bumetanide-sensitive and HCO3--dependent transporters activated by IBMX in renal epithelial A6 cells.
Article in The Journal of membrane biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed, 22 citations in OpenAlex.
- Activation of the Na+-K+ pump by hyposmolality through tyrosine kinase-dependent Cl- conductance in Xenopus renal epithelial A6 cells.The Journal of physiology · 1999Article
- Activation of Na+-permeant cation channel by stretch and cyclic AMP-dependent phosphorylation in renal epithelial A6 cells.The Journal of general physiology · 1997Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We studied cAMP-dependent regulation of ion transport in aldosterone-untreated renal epithelial A6 cells by measuring short-circuit current (Isc). Biphasic increases in Isc, a transient phase followed by a sustained one, were elicited in response to 1 mm 3-isobutyl-1-methylxanthine (IBMX, an inhibitor of phosphodiesterase) which increased cytosolic cAMP concentration. IBMX increased the apical Cl- conductance. The sustained phase of Isc induced by IBMX was reduced by 50 microM bumetanide (Na+/K+/2 Cl- cotransporter inhibitor) or 100 microM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS, an inhibitor of Cl-/HCO3- exchanger). Under the normal condition, the inhibitory effect of bumetanide was much larger than that of DIDS. On the other hand, under a low Cl- condition, the effect of DIDS was more effective than that of bumetanide. Further, under a Cl--free condition Na+/HCO3- symporter contributed to the IBMX-generated Isc. Taken together, our observations suggest that in A6 cells (i) IBMX stimulates Cl- secretion associated with an increase in apical Cl- conductances, (ii) the ionic components to generate the IBMX-induced Isc are mainly maintained by bumetanide-sensitive Na+/K+/2 Cl- cotransporter and DIDS-sensitive Cl-/HCO3- exchanger, (iii) Cl-/HCO3- exchanger coupled to Na+/HCO3- symporter under a low-Cl- condition or Na+/HCO3- symporter under a Cl--free condition contributes to the IBMX-induced Isc, compensating for diminishment of the Na+/K+/2Cl- cotransporter-mediated Cl- secretion, (iv) IBMX increases Cl- and HCO3- conductances in the apical membrane.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.