ArticleBiophysical journal2010
Routes of epithelial water flow: aquaporins versus cotransporters.
Article in Biophysical journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 35 citations in OpenAlex.
- Intraventricular haemorrhage in premature infants: the role of immature neuronal salt and water transport.Brain : a journal of neurology · 2024Article
- From Homeostasis to Pathology: Decoding the Multifaceted Impact of Aquaporins in the Central Nervous System.International journal of molecular sciences · 2023Review
- Roles and regulation of Aquaporin-3 in maintaining the gut health: an updated review.Frontiers in physiology · 2023Review
- Non-Aquaporin Water Channels.Advances in experimental medicine and biology · 2023Article
- Hydrostatic pressure as a driver of cell and tissue morphogenesis.Seminars in cell & developmental biology · 2022Review
- Distribution of aquaporins and sodium transporters in the gastrointestinal tract of a desert hare, Lepus yarkandensis.Scientific reports · 2019Article
- Single-file transport of water through membrane channels.Faraday discussions · 2018Article
- Quantification of Water Flux in Vesicular Systems.Scientific reports · 2018Article
- Chloride Dysregulation, Seizures, and Cerebral Edema: A Relationship with Therapeutic Potential.Trends in neurosciences · 2017Review
- Expression, Distribution and Role of Aquaporin Water Channels in Human and Animal Stomach and Intestines.International journal of molecular sciences · 2016Review
- The Sodium Glucose Cotransporter SGLT1 Is an Extremely Efficient Facilitator of Passive Water Transport.The Journal of biological chemistry · 2016Article
- Detecting Aquaporin Function and Regulation.Frontiers in chemistry · 2016Review
- Novel determinants of the neuronal Cl(-) concentration.The Journal of physiology · 2014Review
- Cotransport of water by Na⁺-K⁺-2Cl⁻ cotransporters expressed in Xenopus oocytes: NKCC1 versus NKCC2.The Journal of physiology · 2012Article
- Monitoring single-channel water permeability in polarized cells.The Journal of biological chemistry · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The routes water takes through membrane barriers is still a matter of debate. Although aquaporins only allow transmembrane water movement along an osmotic gradient, cotransporters are believed to be capable of water transport against the osmotic gradient. Here we show that the renal potassium-chloride-cotransporter (KCC1) does not pump a fixed amount of water molecules per movement of one K(+) and one Cl(-), as was reported for the analogous transporter in the choroid plexus. We monitored water and potassium fluxes through monolayers of primary cultured renal epithelial cells by detecting tiny solute concentration changes in the immediate vicinity of the monolayer. KCC1 extruded K(+) ions in the presence of a transepithelial K(+) gradient, but did not transport water. KCC1 inhibition reduced epithelial osmotic water permeability P(f) by roughly one-third, i.e., the effect of inhibitors was small in resting cells and substantial in hormonal stimulated cells that contained high concentrations of aquaporin-2 in their apical membranes. The furosemide or DIOA (dihydroindenyl-oxy-alkanoic acid)-sensitive water flux was much larger than expected when water passively followed the KCC1-mediated ion flow. The inhibitory effect of these drugs on water flux was reversed by the K(+)-H(+) exchanger nigericin, indicating that KCC1 affects water transport solely by K(+) extrusion. Intracellular K(+) retention conceivably leads to cell swelling, followed by an increased rate of endocytic AQP2 retrieval from the apical membrane.
Indexed as
Identifiers
What OpenQuestion holds
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.