ArticleThe Journal of physiology2013
Genetic ablation of aquaporin-2 in the mouse connecting tubules results in defective renal water handling.
Article in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Molecular mechanisms in lithium-associated renal disease: a systematic review.International urology and nephrology · 2016Pooled it
- Active salt transport and countercurrent exchange as the basis of urine concentration: a proposal grounded on the microanatomy of the renal medulla.Pflugers Archiv : European journal of physiology · 2026Review
- Cannabinoid receptor type 1 activation causes a water diuresis by inducing an acute central diabetes insipidus in mice.American journal of physiology. Renal physiology · 2024Article
- Article
- Renal water transport in health and disease.Pflugers Archiv : European journal of physiology · 2022Review
- Organ Specific Differences in Alteration of Aquaporin Expression in Rats Treated with Sennoside A, Senna Anthraquinones and Rhubarb Anthraquinones.International journal of molecular sciences · 2021Article
- Dietary sodium modulates nephropathy in Nedd4-2-deficient mice.Cell death and differentiation · 2020Article
- Two Mineralocorticoid Receptor-Mediated Mechanisms of Pendrin Activation in Distal Nephrons.Journal of the American Society of Nephrology : JASN · 2020Article
- Generation of Human PSC-Derived Kidney Organoids with Patterned Nephron Segments and a De Novo Vascular Network.Cell stem cell · 2019Article
- The contribution of collecting duct NOS1 to the concentrating mechanisms in male and female mice.American journal of physiology. Renal physiology · 2019Article
- Lack of urea transporters, UT-A1 and UT-A3, increases nitric oxide accumulation to dampen medullary sodium reabsorption through ENaC.American journal of physiology. Renal physiology · 2019Article
- Zika Virus Infection Induces Acute Kidney Injury Through Activating NLRP3 Inflammasome Via Suppressing Bcl-2.Frontiers in immunology · 2019Article
- Progranulin Deficient Mice Develop Nephrogenic Diabetes Insipidus.Aging and disease · 2018Article
- HAmerican journal of physiology. Renal physiology · 2018Article
- Renal tubular NHE3 is required in the maintenance of water and sodium chloride homeostasis.Kidney international · 2017Article
- Role of adenylyl cyclase 6 in the development of lithium-induced nephrogenic diabetes insipidus.JCI insight · 2017Article
- Deficiency of Carbonic Anhydrase II Results in a Urinary Concentrating Defect.Frontiers in physiology · 2017Article
- Nuclear Receptor Regulation of Aquaporin-2 in the Kidney.International journal of molecular sciences · 2016Review
- Autophagic degradation of aquaporin-2 is an early event in hypokalemia-induced nephrogenic diabetes insipidus.Scientific reports · 2015Article
- Dexamethasone increases aquaporin-2 protein expression in ex vivo inner medullary collecting duct suspensions.Frontiers in physiology · 2015Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Body water balance is regulated via the water channel aquaporin-2 (AQP2), which is expressed in the renal connecting tubule (CNT) and collecting duct (CD). The relative roles of AQP2 in the CNT and CD are not fully understood. To study the role of AQP2 in the CNT we generated a mouse model with CNT-specific AQP2 deletion (AQP2-CNT-knockout (KO)). Confocal laser scanning microscopy and immunogold electron microscopy demonstrated an absence of AQP2 in the CNT of AQP2-CNT-KO mice. Twenty-four hour urine output was significantly increased (KO: 3.0 ± 0.3 ml (20 g body weight (BW))(-1); wild-type (WT): 1.9 ± 0.3 ml (20 g BW)(-1)) and urine osmolality decreased (KO: 1179 ± 107 mosmol kg(-1); WT: 1790 ± 146 mosmol kg(-1)) in AQP2-CNT-KO mice compared with controls. After 24 h water restriction, urine osmolality was still significantly lower in AQP2-CNT-KO mice (KO: 2087 ± 169 mosmol kg(-1); WT: 2678 ± 144 mosmol kg(-1)). A significant difference in urine osmolality between groups before desmopressin (dDAVP) (KO: 873 ± 129 mosmol kg(-1); WT: 1387 ± 163 mosmol kg(-1)) was not apparent 2 h after injection, with urine osmolality increased significantly in both groups (KO: 2944 ± 41 mosmol kg(-1); WT: 3133 ± 66 mosmol kg(-1)). Cortical kidney fractions from AQP2-CNT-KO mice had significantly reduced AQP2, with no compensatory changes in sodium potassium chloride cotransporter (NKCC2), AQP3 or AQP4. Lithium chloride treatment increased urine volume and decreased osmolality in both WT and AQP2-CNT-KO mice. After 8 days of treatment, the AQP2-CNT-KO mice still had a significantly higher urine volume and lower urine osmolality, suggesting that the CNT does not play a significant role in the pathology of lithium-induced nephrogenic diabetes insipidus. Our studies indicate that the CNT plays a role in regulating body water balance under basal conditions, but not for maximal concentration of the urine during antidiuresis.
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