ArticleAmerican journal of physiology. Renal physiology2011
Angiotensin II acts through the angiotensin 1a receptor to upregulate pendrin.
Article in American journal of physiology. Renal physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 54 citations in OpenAlex.
- Pendrin is upregulated by corticosterone and participates in its pressor response.American journal of physiology. Renal physiology · 2026Article
- Loss of OXGR1 function uncouples intrarenal RAS activation from pendrin and αENaC regulation and blunts angiotensin II-induced hypertension.Frontiers in pharmacology · 2026Article
- Activation of BK channels ameliorates cardiac injury Via NFκB-NLRP3 signaling in angiotensin II-induced hypertension mouse model.Frontiers in pharmacology · 2026Article
- Pendrin inhibition is associated with protective effect of prone positioning in a ventilator-induced lung injury mouse model.Scientific reports · 2025Article
- Intercalated Cell ClC-K2 Channel Contributes to Systemic ClFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Angiotensin II acts through Rac1 to upregulate pendrin: role of NADPH oxidase.American journal of physiology. Renal physiology · 2024Article
- The K-Cl cotransporter-3 in the mammalian kidney.Current opinion in nephrology and hypertension · 2023Review
- Bicarbonate is the primary inducer of KCC3a expression in renal cortical B-type intercalated cells.American journal of physiology. Cell physiology · 2023Article
- Pendrin abundance, subcellular distribution, and function are unaffected by either αENaC gene ablation or by increasing ENaC channel activity.Pflugers Archiv : European journal of physiology · 2023Article
- Pendrin regulation is prioritized by anion in high-potassium diets.American journal of physiology. Renal physiology · 2023Article
- 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
- 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
- Intercalated Cells of the Kidney Collecting Duct in Kidney Physiology.Seminars in nephrology · 2019Review
- Aldosterone Is Essential for Angiotensin II-Induced Upregulation of Pendrin.Journal of the American Society of Nephrology : JASN · 2018Article
- Renal intercalated cells and blood pressure regulation.Kidney research and clinical practice · 2017Review
- Article
- Effects of Reactive Oxygen Species on Tubular Transport along the Nephron.Antioxidants (Basel, Switzerland) · 2017Review
Corrections and comments
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Authors and funding
14 authors at 7 institutions in 1 country.
Funding
Abstract
Pendrin is an anion exchanger expressed in the apical regions of B and non-A, non-B intercalated cells. Since angiotensin II increases pendrin-mediated Cl(-) absorption in vitro, we asked whether angiotensin II increases pendrin expression in vivo and whether angiotensin-induced hypertension is pendrin dependent. While blood pressure was similar in pendrin null and wild-type mice under basal conditions, following 2 wk of angiotensin II administration blood pressure was 31 mmHg lower in pendrin null than in wild-type mice. Thus pendrin null mice have a blunted pressor response to angiotensin II. Further experiments explored the effect of angiotensin on pendrin expression. Angiotensin II administration shifted pendrin label from the subapical space to the apical plasma membrane, independent of aldosterone. To explore the role of the angiotensin receptors in this response, pendrin abundance and subcellular distribution were examined in wild-type, angiotensin type 1a (Agtr1a) and type 2 receptor (Agtr2) null mice given 7 days of a NaCl-restricted diet (< 0.02% NaCl). Some mice received an Agtr1 inhibitor (candesartan) or vehicle. Both Agtr1a gene ablation and Agtr1 inhibitors shifted pendrin label from the apical plasma membrane to the subapical space, independent of the Agtr2 or nitric oxide (NO). However, Agtr1 ablation reduced pendrin protein abundance through the Agtr2 and NO. Thus angiotensin II-induced hypertension is pendrin dependent. Angiotensin II acts through the Agtr1a to shift pendrin from the subapical space to the apical plasma membrane. This Agtr1 action may be blunted by the Agtr2, which acts through NO to reduce pendrin protein abundance.
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