ArticleJournal of the American Society of Nephrology : JASN2013
Overexpression of pendrin in intercalated cells produces chloride-sensitive hypertension.
Article in Journal of the American Society of Nephrology : JASN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 94 citations in OpenAlex.
- Effect of Sodium Bicarbonate on Indicators of Volume Retention in Metabolic Acidosis After Kidney Transplantation: A Post-Hoc Analysis.Kidney medicine · 2026Article
- Pendrin: linking acid base to blood pressure.Pflugers Archiv : European journal of physiology · 2024Review
- Novel functions of the anion exchanger AE4 (SLC4A9).Pflugers Archiv : European journal of physiology · 2024Review
- ClC-K Kidney Chloride Channels: From Structure to Pathology.Handbook of experimental pharmacology · 2024Article
- SLC26 Anion Transporters.Handbook of experimental pharmacology · 2024Review
- Dietary anions control potassium excretion: it is more than a poorly absorbable anion effect.American journal of physiology. Renal physiology · 2023Article
- Kidney and blood pressure regulation-latest evidence for molecular mechanisms.Clinical kidney journal · 2023Review
- The pathophysiology of distal renal tubular acidosis.Nature reviews. Nephrology · 2023Review
- Review
- Regulation of Blood Pressure and Salt Balance By Pendrin-Positive Intercalated Cells: Donald Seldin Lecture 2020.Hypertension (Dallas, Tex. : 1979) · 2022Review
- Clues and new evidences in arterial hypertension: unmasking the role of the chloride anion.Pflugers Archiv : European journal of physiology · 2022Review
- Characterization of pendrin in urinary extracellular vesicles in a rat model of aldosterone excess and in human primary aldosteronism.Hypertension research : official journal of the Japanese Society of Hypertension · 2021Article
- Renal tubular transport protein regulation in primary aldosteronism: can large-scale proteomic analysis offer a new insight?Journal of human hypertension · 2021Article
- The ClJournal of human hypertension · 2021Article
- 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
- Two Mineralocorticoid Receptor-Mediated Mechanisms of Pendrin Activation in Distal Nephrons.Journal of the American Society of Nephrology : JASN · 2020Article
- Evaluation of the pathophysiological mechanisms of salt-sensitive hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2019Review
- The Molecular Genetics of Gordon Syndrome.Genes · 2019Review
- A Novel Mechanism of Renal Microcirculation Regulation: Connecting Tubule-Glomerular Feedback.Current hypertension reports · 2019Review
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Authors and funding
17 authors at 10 institutions in 3 countries.
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Abstract
Inherited and acquired disorders that enhance the activity of transporters mediating renal tubular Na(+) reabsorption are well established causes of hypertension. It is unclear, however, whether primary activation of an Na(+)-independent chloride transporter in the kidney can also play a pathogenic role in this disease. Here, mice overexpressing the chloride transporter pendrin in intercalated cells of the distal nephron (Tg(B1-hPDS) mice) displayed increased renal absorption of chloride. Compared with normal mice, these transgenic mice exhibited a delayed increase in urinary NaCl and ultimately, developed hypertension when exposed to a high-salt diet. Administering the same sodium intake as NaHCO3 instead of NaCl did not significantly alter BP, indicating that the hypertension in the transgenic mice was chloride-sensitive. Moreover, excessive chloride absorption by pendrin drove parallel absorption of sodium through the epithelial sodium channel ENaC and the sodium-driven chloride/bicarbonate exchanger (Ndcbe), despite an appropriate downregulation of these sodium transporters in response to the expanded vascular volume and hypertension. In summary, chloride transport in the distal nephron can play a primary role in driving NaCl transport in this part of the kidney, and a primary abnormality in renal chloride transport can provoke arterial hypertension. Thus, we conclude that the chloride/bicarbonate exchanger pendrin plays a major role in controlling net NaCl absorption, thereby influencing BP under conditions of high salt intake.
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