ArticleThe Journal of clinical investigation1993
Evidence for conductive Cl- pathway in the basolateral membrane of rabbit renal proximal tubule S3 segment.
Article in The Journal of clinical investigation, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
4 citing papers in PubMed, 19 citations in OpenAlex.
- Regulation of K-Cl cotransport: from function to genes.The Journal of membrane biology · 2004Review
- Chloride transport in the renal proximal tubule.Pflugers Archiv : European journal of physiology · 2004Review
- Pharmacological isolation of the synaptic and nonsynaptic components of the GABA-mediated biphasic response in rat CA1 hippocampal pyramidal cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
- Activation of the basolateral Cl- conductance by cAMP in rabbit renal proximal tubule S3 segments.Pflugers Archiv : European journal of physiology · 1995Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanism of Cl- exit was examined in the basolateral membrane of rabbit renal proximal tubule S3 segment with double-barreled, ion-selective microelectrodes. After the basolateral Cl-/HCO3- exchanger was blocked by 2'-disulfonic acid, a bath K+ step from 5 to 20 mM induced 26.6 mV depolarization and 7.7 mM increase in intracellular Cl- activities ([Cl(-)]i). K+ channel blockers, Ba2+, and quinine strongly suppressed both the response in cell membrane potentials (Vb) and in (Cl-)i to the bath K+ step, while Cl- channel blockers, A9C (1 mM) and IAA-94 (0.3 mM) inhibited only the latter response by 49 and 74%, respectively. By contrast, an inhibitor of K(+)-Cl- cotransporter, H74, had no effect on the increase in (Cl-)i to the bath K+ step. Furosemide and the removal of bath Na+ were also ineffective, suggesting that (Cl-)i are sensitive to the cell potential changes. Bath Cl- removal in the presence of quinine induced a depolarization of more than 10 mV and a decrease in (Cl-)i, and IAA-94 inhibited these responses similarly in the bath K+ step experiments. These results indicate that a significant Cl- conductance exists in the basolateral membrane of this segment and functions as a Cl- exit mechanism.
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