ArticleAmerican journal of physiology. Renal physiology2015
IGF-1 and insulin exert opposite actions on ClC-K2 activity in the cortical collecting ducts.
Article in American journal of physiology. Renal physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- Intercalated Cell ClC-K2 Channel Contributes to Systemic ClFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Review
- ClC-K2 ClFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Inwardly rectifying potassium channel 5.1: Structure, function, and possible roles in diseases.Genes & diseases · 2021Review
- Adenosine inhibits the basolateral ClAmerican journal of physiology. Renal physiology · 2020Article
- Role of ClC-K and barttin in low potassium-induced sodium chloride cotransporter activation and hypertension in mouse kidney.Bioscience reports · 2018Article
- Dietary KPflugers Archiv : European journal of physiology · 2018Article
- (Pro)Renin receptor regulates potassium homeostasis through a local mechanism.American journal of physiology. Renal physiology · 2017Article
- Gastrointestinal-Renal Axis: Role in the Regulation of Blood Pressure.Journal of the American Heart Association · 2017Review
- Role and mechanisms of regulation of the basolateral KActa physiologica (Oxford, England) · 2017Review
- Alkaline activation of ClC-K2 chloride channels switches renal cells from reabsorbing to secreting.The Journal of general physiology · 2016Article
- Dual regulation of the native ClC-K2 chloride channel in the distal nephron by voltage and pH.The Journal of general physiology · 2016Article
- New perspective of ClC-Kb/2 Cl- channel physiology in the distal renal tubule.American journal of physiology. Renal physiology · 2016Review
- Insulin and IGF-1 activate Kir4.1/5.1 channels in cortical collecting duct principal cells to control basolateral membrane voltage.American journal of physiology. Renal physiology · 2016Article
- Implementing Patch Clamp and Live Fluorescence Microscopy to Monitor Functional Properties of Freshly Isolated PKD Epithelium.Journal of visualized experiments : JoVE · 2015Article
- Angiotensin II increases activity of the ClC-K2 ClThe Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Despite similar stimulatory actions on the epithelial sodium channel (ENaC)-mediated sodium reabsorption in the distal tubule, insulin promotes kaliuresis, whereas insulin-like growth factor-1 (IGF-1) causes a reduction in urinary potassium levels. The factors contributing to this phenomenon remain elusive. Electrogenic distal nephron ENaC-mediated Na(+) transport establishes driving force for Cl(-) reabsorption and K(+) secretion. Using patch-clamp electrophysiology, we document that a Cl(-) channel is highly abundant on the basolateral plasma membrane of intercalated cells in freshly isolated mouse cortical collecting duct (CCD) cells. The channel has characteristics attributable to the ClC-K2: slow gating kinetics, conductance ∼10 pS, voltage independence, Cl(-)>NO3 (-) anion selectivity, and inhibition/activation by low/high pH, respectively. IGF-1 (100 and 500 nM) acutely stimulates ClC-K2 activity in a reversible manner. Inhibition of PI3-kinase (PI3-K) with LY294002 (20 μM) abrogates activation of ClC-K2 by IGF-1. Interestingly, insulin (100 nM) reversibly decreases ClC-K2 activity in CCD cells. This inhibitory action is independent of PI3-K and is mediated by stimulation of a mitogen-activated protein kinase-dependent cascade. We propose that IGF-1, by stimulating ClC-K2 channels, promotes net Na(+) and Cl(-) reabsorption, thus reducing driving force for potassium secretion by the CCD. In contrast, inhibition of ClC-K2 by insulin favors coupling of Na(+) reabsorption with K(+) secretion at the apical membrane contributing to kaliuresis.
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Registered trials
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.