ArticleAmerican journal of physiology. Renal physiology2013
Endothelin-1 inhibits sodium reabsorption by ET(A) and ET(B) receptors in the mouse cortical collecting duct.
Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 44 citations in OpenAlex.
- Determining the optimal dose of atrasentan by evaluating the exposure-response relationships of albuminuria and bodyweight.Diabetes, obesity & metabolism · 2018Trial
- Epithelial NaComprehensive Physiology · 2024Review
- Aldosterone: Renal Action and Physiological Effects.Comprehensive Physiology · 2023Article
- Kidney omics in hypertension: from statistical associations to biological mechanisms and clinical applications.Kidney international · 2022Review
- Sex Differences in Diurnal Sodium Handling During Diet-Induced Obesity in Rats.Hypertension (Dallas, Tex. : 1979) · 2022Article
- High salt intake induces collecting duct HDAC1-dependent NO signaling.American journal of physiology. Renal physiology · 2021Article
- Knockout of the circadian clock protein PER1 results in sex-dependent alterations of ET-1 production in mice in response to a high-salt diet plus mineralocorticoid treatment.Canadian journal of physiology and pharmacology · 2020Article
- The rise of circulatory endothelin (ET)-1 and endothelin receptors (ETInternational journal of physiology, pathophysiology and pharmacology · 2019Article
- Thick Ascending Limb Sodium Transport in the Pathogenesis of Hypertension.Physiological reviews · 2019Review
- Nephron prorenin receptor deficiency alters renal medullary endothelin-1 and endothelin receptor expression.Physiological research · 2018Article
- Circadian regulation of renal function.Free radical biology & medicine · 2018Review
- High dietary sodium causes dyssynchrony of the renal molecular clock in rats.American journal of physiology. Renal physiology · 2018Article
- ENaC activity in the cortical collecting duct of HKαAmerican journal of physiology. Renal physiology · 2017Article
- Endothelin-1 mediates natriuresis but not polyuria during vitamin D-induced acute hypercalcaemia.The Journal of physiology · 2017Article
- Aldosterone alters the chromatin structure of the murine endothelin-1 gene.Life sciences · 2016Article
- Role of the Renin-Angiotensin-Aldosterone System beyond Blood Pressure Regulation: Molecular and Cellular Mechanisms Involved in End-Organ Damage during Arterial Hypertension.International journal of molecular sciences · 2016Review
- Effect of mineralocorticoid treatment in mice with collecting duct-specific knockout of endothelin-1.American journal of physiology. Renal physiology · 2015Article
- The Circadian Clock in the Regulation of Renal Rhythms.Journal of biological rhythms · 2015Review
- Chloride secretion by renal collecting ducts.Current opinion in nephrology and hypertension · 2015Article
- Endothelin-1 critically influences cardiac function via superoxide-MMP9 cascade.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
The collecting duct (CD) is a major renal site for the hormonal regulation of Na homeostasis and is critical for systemic arterial blood pressure control. Our previous studies demonstrated that the endothelin-1 gene (edn1) is an early response gene to the action of aldosterone. Because aldosterone and endothelin-1 (ET-1) have opposing actions on Na reabsorption (JNa) in the kidney, we postulated that stimulation of ET-1 by aldosterone acts as a negative feedback mechanism, acting locally within the CD. Aldosterone is known to increase JNa in the CD, in part, by stimulating the epithelial Na channel (ENaC). In contrast, ET-1 increases Na and water excretion through its binding to receptors in the CD. To date, direct measurement of the quantitative effect of ET-1 on transepithelial JNa in the isolated in vitro microperfused mouse CD has not been determined. We observed that the CD exhibits substantial JNa in male and female mice that is regulated, in part, by a benzamil-sensitive pathway, presumably ENaC. ENaC-mediated JNa is greater in the cortical CD (CCD) than in the outer medullary CD (OMCD); however, benzamil-insensitive JNa is present in the CCD and not in the OMCD. In the presence of ET-1, ENaC-mediated JNa is significantly inhibited. Blockade of either ETA or ETB receptor restored JNa to control rates; however, only ETA receptor blockade restored a benzamil-sensitive component of JNa. We conclude 1) Na reabsorption is mediated by ENaC in the CCD and OMCD and also by an ENaC-independent mechanism in the CCD; and 2) ET-1 inhibits JNa in the CCD through both ETA and ETB receptor-mediated pathways.
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