ArticleThe Journal of clinical investigation2001
Endothelin-1/endothelin-B receptor-mediated increases in NHE3 activity in chronic metabolic acidosis.
Article in The Journal of clinical investigation, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 94 citations in OpenAlex.
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- Endothelin receptors in renal interstitial cells do not contribute to the development of fibrosis during experimental kidney disease.Pflugers Archiv : European journal of physiology · 2021Article
- Alkali supplementation as a therapeutic in chronic kidney disease: what mediates protection?American journal of physiology. Renal physiology · 2020Review
- Acetazolamide causes renalAmerican journal of physiology. Renal physiology · 2020Article
- Testosterone modulates renal ammonia metabolism.American journal of physiology. Renal physiology · 2020Article
- Acid-base regulation in the renal proximal tubules: using novel pH sensors to maintain homeostasis.American journal of physiology. Renal physiology · 2018Review
- Differences in renal ammonia metabolism in male and female kidney.American journal of physiology. Renal physiology · 2018Article
- Chronic lithium treatment induces novel patterns of pendrin localization and expression.American journal of physiology. Renal physiology · 2018Article
- Acid Stimulation of the Citrate Transporter NaDC-1 Requires Pyk2 and ERK1/2 Signaling Pathways.Journal of the American Society of Nephrology : JASN · 2018Article
- Zebrafish as a Model System for Investigating the Compensatory Regulation of Ionic Balance during Metabolic Acidosis.International journal of molecular sciences · 2018Review
- Dopamine reduces cell surface NaAmerican journal of physiology. Renal physiology · 2017Article
- Ammonia Transporters and Their Role in Acid-Base Balance.Physiological reviews · 2017Review
- Acidosis and Urinary Calcium Excretion: Insights from Genetic Disorders.Journal of the American Society of Nephrology : JASN · 2016Review
- Proximal tubule-specific glutamine synthetase deletion alters basal and acidosis-stimulated ammonia metabolism.American journal of physiology. Renal physiology · 2016Article
- Dual inhibition of renin-angiotensin-aldosterone system and endothelin-1 in treatment of chronic kidney disease.American journal of physiology. Regulatory, integrative and comparative physiology · 2016Review
- Immunolocalization of hyperpolarization-activated cationic HCN1 and HCN3 channels in the rat nephron: regulation of HCN3 by potassium diets.Histochemistry and cell biology · 2016Article
- Endothelin Blockade in Diabetic Kidney Disease.Journal of clinical medicine · 2015Review
- Endothelin and renal ion and water transport.Seminars in nephrology · 2015Review
- Molecular mechanisms and regulation of urinary acidification.Comprehensive Physiology · 2014Review
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Authors and funding
5 authors at 3 institutions in 1 country.
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Abstract
Decreases in blood pH activate NHE3, the proximal tubular apical membrane Na/H antiporter. In cultured renal epithelial cells, activation of the endothelin-B (ET(B)) receptor increases NHE3 activity. To examine the role of the ET(B) receptor in the response to acidosis in vivo, the present studies examined ET(B) receptor-deficient mice, rescued from neonatal lethality by expression of a dopamine beta-hydroxylase promoter/ET(B) receptor transgene (Tg/Tg:ET(B)(-/-) mice). In proximal tubule suspensions from Tg/Tg:ET(B)(+/-) mice, 10(-8) M endothelin-1 (ET-1) increased NHE3 activity, but this treatment had no effect on tubules from Tg/Tg:ET(B)(-/-) mice. Acid ingestion for 7 days caused a greater decrease in blood HCO(3)(-) concentration in Tg/Tg:ET(B)(-/-) mice compared with Tg/Tg:ET(B)(+/+) and Tg/Tg:ET(B)(+/-) mice. Whereas acid ingestion increased apical membrane NHE3 by 42-46% in Tg/Tg:ET(B)(+/+) and Tg/Tg:ET(B)(+/-) mice, it had no effect on NHE3 in Tg/Tg:ET(B)(-/-) mice. In C57BL/6 mice, excess acid ingestion increased renal cortical preproET-1 mRNA expression 2.4-fold and decreased preproET-3 mRNA expression by 37%. On a control diet, Tg/Tg:ET(B)(-/-) mice had low rates of ammonium excretion, which could not be attributed to an inability to acidify the urine, as well as hypercitraturia, with increased titratable acid excretion. Acid ingestion increased ammonium excretion, citrate absorption, and titratable acid excretion to the same levels in Tg/Tg:ET(B)(-/-) and Tg/Tg:ET(B)(+/+) mice. In conclusion, metabolic acidosis increases ET-1 expression, which increases NHE3 activity via the ET(B) receptor.
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