ArticleThe Journal of physiology1997
Inwardly rectifying, voltage-dependent and resting potassium currents in rat pancreatic acinar cells in primary culture.
Article in The Journal of physiology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 18 citations in OpenAlex.
- Article
- CO2-dependent opening of an inwardly rectifying K+ channel.Pflugers Archiv : European journal of physiology · 2011Article
- Delayed expression of large conductance K+ channels reshaping agonist-induced currents in mouse pancreatic acinar cells.The Journal of physiology · 2005Article
- Pancreatic two P domain K+ channels TALK-1 and TALK-2 are activated by nitric oxide and reactive oxygen species.The Journal of physiology · 2005Article
- General anesthetic octanol and related compounds activate wild-type and delF508 cystic fibrosis chloride channels.British journal of pharmacology · 2004Article
- Characterization of cell volume-sensitive chloride currents in freshly prepared and cultured pancreatic acinar cells from early postnatal rats.The Journal of physiology · 1998Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. In exocrine pancreatic acinar cells in primary culture an inwardly rectifying, a voltage-dependent and a permanent resting K+ current were characterized. 2. Inwardly rectifying K+ currents could be elicited by elevation of the extracellular K+ concentration. The K+ inward currents were almost completely blocked by 5 mM Ba2+, whereas 10 mM TEA+ had only a partial effect. 3. Depolarizing voltage steps from negative clamp potentials evoked transient activation of a voltage-dependent K+ current. This voltage-dependent current could be blocked by 10 mM TEA+ and 1 mM 4-aminopyridine, but not by 5 mM Ba2+. 4. Neither the K+ inward rectifier nor the voltage-dependent K+ conductance produced a significant negative cell potential. Stable membrane potentials (-38.7 +/- 2.3 mV, n = 38) could only be recorded on cell clusters (> or = 5 cells). 5. Cell clusters, in contrast to single cells, had a permanent resting K+ conductance in addition to the inward rectifier and the voltage-dependent current. This resting K+ conductance was not blocked by TEA+, Ba2+, 4-aminopyridine or by the chromanol 293B. 6. Cytosolic alkalization by addition of NH4Cl to the bath solution decreased the resting K+ current. In parallel, electrical uncoupling of the cells and breakdown of the resting potential could be observed. The same effects could be produced when the cells were uncoupled by 0.2-1.0 mM n-octanol. It can be concluded that cell coupling is essential for maintenance of stable resting membrane potentials in pancreatic acinar cells.
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