ReviewAmerican journal of physiology. Renal physiology2013
Novel diuretic targets.
Review in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 33 citations in OpenAlex.
- Mechanism of Gating and Isoform-Specific Inhibition in Renal CLC Chloride Channels.bioRxiv : the preprint server for biology · 2026Article
- Inwardly rectifying potassium channels: Critical insights for insect species and Apis mellifera.Channels (Austin, Tex.) · 2025Review
- ClC-K Kidney Chloride Channels: From Structure to Pathology.Handbook of experimental pharmacology · 2024Article
- Special collection on inward rectifying KAmerican journal of physiology. Cell physiology · 2023Article
- VU6036720: The First Potent and Selective In Vitro Inhibitor of Heteromeric Kir4.1/5.1 Inward Rectifier Potassium Channels.Molecular pharmacology · 2022Article
- Phylogenomics of Tick Inward Rectifier Potassium Channels and Their Potential as Targets to Innovate Control Technologies.Frontiers in cellular and infection microbiology · 2021Review
- Complementary computational and experimental evaluation of missense variants in the ROMK potassium channel.PLoS computational biology · 2020Article
- AMP-Activated Protein Kinase (AMPK)-Dependent Regulation of Renal Transport.International journal of molecular sciences · 2018Review
- Discovery, Characterization, and Effects on Renal Fluid and Electrolyte Excretion of the Kir4.1 Potassium Channel Pore Blocker, VU0134992.Molecular pharmacology · 2018Article
- A selective class of inhibitors for the CLC-Ka chloride ion channel.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Discovery and in Vitro Optimization of 3-Sulfamoylbenzamides as ROMK Inhibitors.ACS medicinal chemistry letters · 2018Article
- Plight of the pore polar bar(rier).Channels (Austin, Tex.) · 2017Article
- Pore Polarity and Charge Determine Differential Block of Kir1.1 and Kir7.1 Potassium Channels by Small-Molecule Inhibitor VU590.Molecular pharmacology · 2017Article
- In silico model of the human ClC-Kb chloride channel: pore mapping, biostructural pathology and drug screening.Scientific reports · 2017Article
- Pharmacovigilance database search discloses ClC-K channels as a novel target of the ATBritish journal of pharmacology · 2017Article
- Article
- ML418: The First Selective, Sub-Micromolar Pore Blocker of Kir7.1 Potassium Channels.ACS chemical neuroscience · 2016Article
- ROMK inhibitor actions in the nephron probed with diuretics.American journal of physiology. Renal physiology · 2016Article
- 13C NMR detects conformational change in the 100-kD membrane transporter ClC-ec1.Journal of biomolecular NMR · 2015Article
- Diuresis and reduced urinary osmolality in rats produced by small-molecule UT-A-selective urea transport inhibitors.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
As the molecular revolution continues to inform a deeper understanding of disease mechanisms and pathways, there exist unprecedented opportunities for translating discoveries at the bench into novel therapies for improving human health. Despite the availability of several different classes of antihypertensive medications, only about half of the 67 million Americans with hypertension manage their blood pressure appropriately. A broader selection of structurally diverse antihypertensive drugs acting through different mechanisms would provide clinicians with greater flexibility in developing effective treatment regimens for an increasingly diverse and aging patient population. An emerging body of physiological, genetic, and pharmacological evidence has implicated several renal ion-transport proteins, or regulators thereof, as novel, yet clinically unexploited, diuretic targets. These include the renal outer medullary potassium channel, ROMK (Kir1.1), Kir4.1/5.1 potassium channels, ClC-Ka/b chloride channels, UTA/B urea transporters, the chloride/bicarbonate exchanger pendrin, and the STE20/SPS1-related proline/alanine-rich kinase (SPAK). The molecular pharmacology of these putative targets is poorly developed or lacking altogether; however, recent efforts by a few academic and pharmaceutical laboratories have begun to lessen this critical barrier. Here, we review the evidence in support of the aforementioned proteins as novel diuretic targets and highlight examples where progress toward developing small-molecule pharmacology has been made.
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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.