ArticleProceedings of the National Academy of Sciences of the United States of America2006
Severe urinary concentrating defect in renal collecting duct-selective AQP2 conditional-knockout mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed, 168 citations in OpenAlex.
- Abnormal function of the vasopressin-cyclic-AMP-aquaporin2 axis during urine concentrating and diluting in patients with reduced renal function. A case control study.BMC nephrology · 2010Trial
- Transcriptional regulatory factors of the Aqp2 gene.Kidney research and clinical practice · 2026Article
- Repeated heat exposure upregulates skeletal muscle aquaporin-4 expression in male mice.Physiological reports · 2026Article
- Regulation of renal aquaporins: implications in tubular epithelial integrity.Biochemical Society transactions · 2026Review
- Lysine acetylation of aquaporin-3 promotes water permeability but is not essential for urine concentrating ability.American journal of physiology. Renal physiology · 2025Article
- Uric acid reduces the expression of aquaporins in renal collecting ducts to increase urine output in hyperuricemia.Frontiers in physiology · 2025Article
- Urinary podocyte stress marker as a prognostic indicator for diabetic kidney disease.BMC nephrology · 2024Article
- Role of EP4 factor in paediatric type 1 diabetes mellitus: a comprehensive review focusing on the honeymoon period.Pediatric endocrinology, diabetes, and metabolism · 2024Review
- Methods for studying mammalian aquaporin biology.Biology methods & protocols · 2023Review
- Aquaporins in Urinary System.Advances in experimental medicine and biology · 2023Article
- Article
- Renal water transport in health and disease.Pflugers Archiv : European journal of physiology · 2022Review
- Signaling Mechanisms and Pharmacological Modulators Governing Diverse Aquaporin Functions in Human Health and Disease.International journal of molecular sciences · 2022Review
- A possible critical dosing period of p-cumylphenol for development of cystic kidneys in rat neonates.Journal of toxicologic pathology · 2022Article
- Connexin mRNA distribution in adult mouse kidneys.Pflugers Archiv : European journal of physiology · 2021Article
- Article
- Pax2 and Pax8 Proteins Regulate Urea Transporters and Aquaporins to Control Urine Concentration in the Adult Kidney.Journal of the American Society of Nephrology : JASN · 2020Article
- Quantitative Proteomics of All 14 Renal Tubule Segments in Rat.Journal of the American Society of Nephrology : JASN · 2020Article
- New insights into the transcriptional regulation of aquaporin-2 and the treatment of X-linked hereditary nephrogenic diabetes insipidus.Kidney research and clinical practice · 2019Article
- Vasopressin-aquaporin-2 pathway: recent advances in understanding water balance disorders.F1000Research · 2019Review
20 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aquaporin-2 (AQP2) is the predominant vasopressin-regulated water channel in kidney connecting tubule (CNT) and collecting duct (CD) and is essential for renal regulation of body water balance. However, the relative role of AQP2 to urinary concentration in the CNT and CD segments is unknown. To examine this directly, transgenic mice expressing AQP2 selectively in CNT but lacking AQP2 expression in CD (AQP2-CD-KO) and mice lacking AQP2 globally (AQP2-total-KO) were generated by exploiting the Cre/loxP technology. LoxP sites were inserted into AQP2 introns 2 and 3, and transgenic mice were bred with strains expressing Cre recombinase under the control of CD-specific Hoxb7- or global EIIa promoter. Mice lacking AQP2 globally died postnatally (days 5-12). AQP2-CD-KO mice were viable to adulthood and showed decreased body weight, 10-fold increased urine production (0.96 +/- 0.11 vs. 0.10 +/- 0.01 ml/g of body weight), and decreased urinary osmolality (170 +/- 19 vs. 1,630 +/- 135 milliosmoles/kg of H(2)O). Immunohistochemical staining of AQP2-CD-KO kidneys (n = 12) revealed sustained, strong AQP2 expression in CNT cells, whereas >95% of CD principal cells were completely AQP2-negative. Water deprivation for 3 hours caused only marginal decreased urine output (87 +/- 7% of levels when mice had free water access; P = 0.04) with no change in urine osmolality, revealing an absence of compensatory mechanisms. These results demonstrate that AQP2 in CNT is sufficient for postnatal survival and that AQP2 in CD is essential for regulation of body water balance and cannot be compensated for by other mechanisms.
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