ReviewClinical and experimental nephrology2012
Renal outer medullary potassium channel knockout models reveal thick ascending limb function and dysfunction.
Review in Clinical and experimental nephrology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Evaluation of the direct effect of remote ischemic preconditioning on the rabbit's kidney by RBMC medical imaging · 2026Article
- Global knockout of ROMK potassium channel worsens cardiac ischemia-reperfusion injury but cardiomyocyte-specific knockout does not: Implications for the identity of mitoKATP.Journal of molecular and cellular cardiology · 2020Article
- Urinary bladder hypertrophy characteristic of male ROMK Bartter's mice does not occur in female mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2018Article
- Potential of Renal Outer Medullary Potassium (ROMK) Channel as Treatments for Hypertension and Heart Failure.ACS medicinal chemistry letters · 2017Article
- Romk1 Knockout Mice Do Not Produce Bartter Phenotype but Exhibit Impaired K Excretion.The Journal of biological chemistry · 2016Article
- Article
- Cesium-associated hypokalemia successfully treated with amiloride.Clinical kidney journal · 2015Article
- Inward-rectifying potassium channelopathies: new insights into disorders of sodium and potassium homeostasis.Pediatric nephrology (Berlin, Germany) · 2015Review
- Evidence of K+ channel function in epithelial cell migration, proliferation, and repair.American journal of physiology. Cell physiology · 2014Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The renal outer medullary potassium channel (ROMK) is an adenosine triphosphate-sensitive inward-rectifier potassium channel (Kir1.1 or KCNJ1) highly expressed in the cortical and medullary thick ascending limbs (TAL), connecting segment (CNT) and cortical collecting duct (CCD) in the mammalian kidney, where it serves to recycle potassium (K(+)) across the apical membrane in TAL and to secrete K(+) in the CNT and CCD. ROMK channel mutations cause type II Bartter's syndrome with salt wasting and dehydration, and ROMK knockout mice display a similar phenotype of Bartter's syndrome in humans. Studies from ROMK null mice indicate that ROMK is required to form both the small-conductance (30pS, SK) K channels and the 70pS (IK) K channels in the TAL. The availability of ROMK(-/-) mice has made it possible to study electrolyte transport along the nephron in order to understand the TAL function under physiological conditions and the compensatory mechanisms of salt and water transport under the conditions of TAL dysfunction. This review summarizes previous progress in the study of K(+) channel activity in the TAL and CCD, ion transporter expression and activities along the nephron, and renal functions under physiological and pathophysiological conditions using ROMK(-/-) mice.
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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.