ArticleThe Journal of clinical investigation2013
Renal β-intercalated cells maintain body fluid and electrolyte balance.
Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 122 citations in OpenAlex.
- Resolving cell-cell interaction networks and their molecular logic in complex tissues.Nature methods · 2026Article
- Urinary sodium wasting and disrupted collecting duct function in mice with distal renal tubular acidosis mutations.Disease models & mechanisms · 2025Article
- Diuretics in patients with chronic kidney disease.Nature reviews. Nephrology · 2025Review
- Revisiting voltage-coupled HAmerican journal of physiology. Renal physiology · 2024Review
- Collecting Duct Pro(Renin) Receptor Contributes to Unilateral Ureteral Obstruction-Induced Kidney Injury via Activation of the Intrarenal RAS.Hypertension (Dallas, Tex. : 1979) · 2024Article
- Intercalated cell function, kidney innate immunity, and urinary tract infections.Pflugers Archiv : European journal of physiology · 2024Review
- Pendrin: linking acid base to blood pressure.Pflugers Archiv : European journal of physiology · 2024Review
- Mechanisms and physiological relevance of acid-base exchange in functional units of the kidney.PeerJ · 2024Review
- β3-Adrenoceptor as a new player in the sympathetic regulation of the renal acid-base homeostasis.Frontiers in physiology · 2024Article
- Potential Theranostic Roles of SLC4 Molecules in Human Diseases.International journal of molecular sciences · 2023Review
- The pathophysiology of distal renal tubular acidosis.Nature reviews. Nephrology · 2023Review
- Mechanistic insights into the primary and secondary alterations of renal ion and water transport in the distal nephron.Journal of internal medicine · 2023Review
- Cell-Specific Actions of the Prostaglandin E-Prostanoid Receptor 4 Attenuating Hypertension: A Dominant Role for Kidney Epithelial Cells Compared With Macrophages.Journal of the American Heart Association · 2022Article
- Distal renal tubular acidosis presenting with an acute hypokalemic paralysis in an older child with severe vesicoureteral reflux and syringomyelia: a case report.BMC nephrology · 2022Article
- Pendrin-null mice develop severe hypokalemia following dietary NaAmerican journal of physiology. Renal physiology · 2022Article
- Regulation of Blood Pressure and Salt Balance By Pendrin-Positive Intercalated Cells: Donald Seldin Lecture 2020.Hypertension (Dallas, Tex. : 1979) · 2022Review
- Renal Tubular Acidosis and Management Strategies: A Narrative Review.Advances in therapy · 2021Review
- Adaptive response of the murine collecting duct to alkali loading.Pflugers Archiv : European journal of physiology · 2020Article
- The Renal Physiology of Pendrin-Positive Intercalated Cells.Physiological reviews · 2020Review
- Intercalated cell BKα subunit is required for flow-induced K+ secretion.JCI insight · 2020Article
10 more citing papers are in PubMed but not listed here.
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10 authors at 4 institutions in 3 countries.
Funding
Abstract
Inactivation of the B1 proton pump subunit (ATP6V1B1) in intercalated cells (ICs) leads to type I distal renal tubular acidosis (dRTA), a disease associated with salt- and potassium-losing nephropathy. Here we show that mice deficient in ATP6V1B1 (Atp6v1b1-/- mice) displayed renal loss of NaCl, K+, and water, causing hypovolemia, hypokalemia, and polyuria. We demonstrated that NaCl loss originated from the cortical collecting duct, where activity of both the epithelial sodium channel (ENaC) and the pendrin/Na(+)-driven chloride/bicarbonate exchanger (pendrin/NDCBE) transport system was impaired. ENaC was appropriately increased in the medullary collecting duct, suggesting a localized inhibition in the cortex. We detected high urinary prostaglandin E2 (PGE2) and ATP levels in Atp6v1b1-/- mice. Inhibition of PGE2 synthesis in vivo restored ENaC protein levels specifically in the cortex. It also normalized protein levels of the large conductance calcium-activated potassium channel and the water channel aquaporin 2, and improved polyuria and hypokalemia in mutant mice. Furthermore, pharmacological inactivation of the proton pump in β-ICs induced release of PGE2 through activation of calcium-coupled purinergic receptors. In the present study, we identified ATP-triggered PGE2 paracrine signaling originating from β-ICs as a mechanism in the development of the hydroelectrolytic imbalance associated with dRTA. Our data indicate that in addition to principal cells, ICs are also critical in maintaining sodium balance and, hence, normal vascular volume and blood pressure.
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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.