ArticleProceedings of the National Academy of Sciences of the United States of America2004
Proximal renal tubular acidosis in TASK2 K+ channel-deficient mice reveals a mechanism for stabilizing bicarbonate transport.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
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Who cites it
78 citing papers in PubMed, 135 citations in OpenAlex.
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- A Comparative Kidney Transcriptome Analysis of Bicarbonate-LoadedCurrent issues in molecular biology · 2023Article
- Genetic Diagnosis and Treatment of Inherited Renal Tubular Acidosis.Kidney diseases (Basel, Switzerland) · 2023Review
- Synergistic effects of agonists and two-pore-domain potassium channels on secretory responses of human pancreatic duct cells Capan-1.Pflugers Archiv : European journal of physiology · 2023Article
- Criteria for central respiratory chemoreceptors: experimental evidence supporting current candidate cell groups.Frontiers in physiology · 2023Review
- TWIK-related acid-sensitive KiScience · 2022Article
- Directing two-way traffic in the kidney: A tale of two ions.The Journal of general physiology · 2022Article
- Genetic variants in eleven central and peripheral chemoreceptor genes in sudden infant death syndrome.Pediatric research · 2022Article
- Kidney metabolism and acid-base control: back to the basics.Pflugers Archiv : European journal of physiology · 2022Review
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18 more citing papers are in PubMed but not listed here.
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15 authors.
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Abstract
The acid- and volume-sensitive TASK2 K+ channel is strongly expressed in renal proximal tubules and papillary collecting ducts. This study was aimed at investigating the role of TASK2 in renal bicarbonate reabsorption by using the task2 -/- mouse as a model. After backcross to C57BL6, task2 -/- mice showed an increased perinatal mortality and, in adulthood, a reduced body weight and arterial blood pressure. Patch-clamp experiments on proximal tubular cells indicated that TASK2 was activated during HCO3- transport. In control inulin clearance measurements, task2 -/- mice showed normal NaCl and water excretion. During i.v. NaHCO3 perfusion, however, renal Na+ and water reabsorption capacity was reduced in -/- animals. In conscious task2 -/- mice, blood pH, HCO3- concentration, and systemic base excess were reduced but urinary pH and HCO3- were increased. These data suggest that task2 -/- mice exhibit metabolic acidosis caused by renal loss of HCO3-. Both in vitro and in vivo results demonstrate the specific coupling of TASK2 activity to HCO3- transport through external alkalinization. The consequences of the task2 gene inactivation in mice are reminiscent of the clinical manifestations seen in human proximal renal tubular acidosis syndrome.
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