ArticleThe Journal of clinical investigation1996
Endothelin(B) receptor activates NHE-3 by a Ca2+-dependent pathway in OKP cells.
Article in The Journal of clinical investigation, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 68 citations in OpenAlex.
- Na/K-ATPase in the renal proximal tubule cell: classic & novel roles in sodium handling.Frontiers in physiology · 2026Review
- 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
- NaThe Journal of physiology · 2017Article
- Article
- Endothelin Blockade in Diabetic Kidney Disease.Journal of clinical medicine · 2015Review
- Molecular mechanisms and regulation of urinary acidification.Comprehensive Physiology · 2014Review
- Proximal nephron.Comprehensive Physiology · 2013Review
- Physiology of endothelin and the kidney.Comprehensive Physiology · 2011Review
- Activation of Na+/H+ exchanger NHE3 by angiotensin II is mediated by inositol 1,4,5-triphosphate (IP3) receptor-binding protein released with IP3 (IRBIT) and Ca2+/calmodulin-dependent protein kinase II.The Journal of biological chemistry · 2010Article
- Mechanisms of the regulation of the intestinal Na+/H+ exchanger NHE3.Journal of biomedicine & biotechnology · 2010Review
- Luminal Na(+)/H (+) exchange in the proximal tubule.Pflugers Archiv : European journal of physiology · 2009Review
- IRBIT, inositol 1,4,5-triphosphate (IP3) receptor-binding protein released with IP3, binds Na+/H+ exchanger NHE3 and activates NHE3 activity in response to calcium.The Journal of biological chemistry · 2008Article
- Na+/H+ exchangers in renal regulation of acid-base balance.Seminars in nephrology · 2006Review
- Increased endothelin activity mediates augmented distal nephron acidification induced by dietary protein.Transactions of the American Clinical and Climatological Association · 2005Article
- Dietary acid, endothelins, and sleep.Transactions of the American Clinical and Climatological Association · 2004Article
- Endothelin-1/endothelin-B receptor-mediated increases in NHE3 activity in chronic metabolic acidosis.The Journal of clinical investigation · 2001Article
- Endogenous endothelins mediate increased distal tubule acidification induced by dietary acid in rats.The Journal of clinical investigation · 1997Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
To examine the mechanisms by which endothelin (ET) regulates the Na/H antiporter isoform, NHE-3, OKP cells were stably transfected with ET(A) and ET(B) receptor cDNA. In cells overexpressing ET(B), but not ET(A) receptors, ET-1 increased Na/H antiporter activity (JNa/H). This effect was inhibited by a nonselective endothelin receptor blocker and by a selective ET(B) receptor blocker but was not inhibited by an ET(A) selective receptor blocker. In ET(B)-overexpressing cells, 10(-8) M ET-1 inhibited adenylyl cyclase, but protein kinase A inhibition and pertussis toxin pretreatment did not affect Na/H antiporter activation by ET-1. ET-1 caused a transient increase in cell [Ca2+], followed by a sustained increase. Increases in cell [Ca2+] were partially inhibited by pertussis toxin. ET-1-induced increases in J(Na/H) were 50% inhibited by clamping cell [Ca2+] low with BAPTA, and by KN62, a Ca-calmodulin kinase inhibitor. Inhibitors of protein kinase C, cyclooxygenase, lipoxygenase, and cytochrome P450 and cyclic GMP were without effect. In ET(A)-overexpressing cells, ET-1 increased cell [Ca2+] but did not increase JNa/H. In summary, binding of ET-1 to ET(B) receptors increases Na/H antiporter activity in OKP cells, an effect mediated in part by increases in cell [Ca2+] and Ca-calmodulin kinase. Increases in cell [Ca2+] are not sufficient for Na/H antiporter activation.
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