Actions of endothelin-1 on calcium homeostasis in Madin—Darby canine kidney tubule cells
Identifieur interne : 002114 ( Main/Exploration ); précédent : 002113; suivant : 002115Actions of endothelin-1 on calcium homeostasis in Madin—Darby canine kidney tubule cells
Auteurs : N. A. Parkinson [Royaume-Uni] ; A. F. James [Royaume-Uni] ; B. M. Hendry [Royaume-Uni]Source :
- Nephrology Dialysis Transplantation [ 0931-0509 ] ; 1996-08.
Abstract
Background. In both ischaemic and nephrotoxic models, renal failure is associated with increased endothelin-l (ET-1) and cell calcium overload, and ET receptor antagonists are protective. Vascular and tubular actions of endothelins appear to be involved. This study examines the actions of ET-1 on intracellular Ca ([Ca2+]i) in the tubule model cell line MDCK (Madin-Darby canine kidney). Methods. Single-cell [Ca2+]i was measured using fura-2 and actions of ET-1 were compared with thapsigargin, which empties IP3-sensitive intracellular Ca stores. Results. Mean resting [Ca2+]i was 84 nM (s.e.m. 6, n=87). 1 μM thapsigargin and 100 nM ET-1 each caused a transient increase in [Ca2+]i by 696 nM (s.e.m. 160, n=9) and 727 nM (s.e.m. 121, n=5) respectively. After 1 μM thapsigargin, 100 nM ET-1 had no effect on [Ca2+]i Oscillations in [Ca2+]i were frequently observed following 100 nM ET-1. In Ca2+-free extracellular solution, mean resting [Ca2+]i was reduced by 37 nM (s.e.m. 5, n=11) and the mean transient increase in [Ca2+]i in response to ET-1 was 419 nM (s.e.m. 97, n=5). Inhibition of the plasma membrane Ca-ATPase with La3+ halved the rate of [Ca2+]i removal from the cytoplasm following ET-1. The PKC inhibitor, chelerythrine (1 μM), reduced the ET-1 induced increase in [Ca2+]i to 349 nM (s.e.m. 97, n=5) and also reduced the rate of removal of [Ca2+]i Ligand binding studies demonstrated ETA receptor expression in MDCK cells sensitive to ET-1. Conclusions. ET-1 releases Ca2+ from IP3-sensitive stores in MDCK cells as well as stimulating extracellular Ca2+ entry leading to oscillations of [Ca2+]i. Ca2+ responses to ET-1 are potentiated by PKC; the plasma membrane Ca ATPase contributes to removal of Ca2+ from the cytoplasm.
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DOI: 10.1093/oxfordjournals.ndt.a027608
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Hendry</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:C18EEB1838F1FFF350118F980A81FBBAEED86476</idno><date when="1996" year="1996">1996</date><idno type="doi">10.1093/oxfordjournals.ndt.a027608</idno><idno type="url">https://api.istex.fr/document/C18EEB1838F1FFF350118F980A81FBBAEED86476/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">002E90</idno><idno type="wicri:Area/Main/Curation">002B04</idno><idno type="wicri:Area/Main/Exploration">002114</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Actions of endothelin-1 on calcium homeostasis in Madin—Darby canine kidney tubule cells</title><author><name sortKey="Parkinson, N A" sort="Parkinson, N A" uniqKey="Parkinson N" first="N. A." last="Parkinson">N. A. Parkinson</name><affiliation wicri:level="3"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Renal Group, Department of Medicine, Kings College School of Medicine & Dentistry, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author><author><name sortKey="James, A F" sort="James, A F" uniqKey="James A" first="A. F." last="James">A. F. James</name><affiliation wicri:level="3"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Renal Group, Department of Medicine, Kings College School of Medicine & Dentistry, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author><author><name sortKey="Hendry, B M" sort="Hendry, B M" uniqKey="Hendry B" first="B. M." last="Hendry">B. M. Hendry</name><affiliation wicri:level="3"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Renal Group, Department of Medicine, Kings College School of Medicine & Dentistry, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Nephrology Dialysis Transplantation</title><idno type="ISSN">0931-0509</idno><idno type="eISSN">1460-2385</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="1996-08">1996-08</date><biblScope unit="volume">11</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="1532">1532</biblScope><biblScope unit="page" to="1537">1537</biblScope></imprint><idno type="ISSN">0931-0509</idno></series><idno type="istex">C18EEB1838F1FFF350118F980A81FBBAEED86476</idno><idno type="DOI">10.1093/oxfordjournals.ndt.a027608</idno><idno type="ArticleID">11.8.1532</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0931-0509</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Background. In both ischaemic and nephrotoxic models, renal failure is associated with increased endothelin-l (ET-1) and cell calcium overload, and ET receptor antagonists are protective. Vascular and tubular actions of endothelins appear to be involved. This study examines the actions of ET-1 on intracellular Ca ([Ca2+]i) in the tubule model cell line MDCK (Madin-Darby canine kidney). Methods. Single-cell [Ca2+]i was measured using fura-2 and actions of ET-1 were compared with thapsigargin, which empties IP3-sensitive intracellular Ca stores. Results. Mean resting [Ca2+]i was 84 nM (s.e.m. 6, n=87). 1 μM thapsigargin and 100 nM ET-1 each caused a transient increase in [Ca2+]i by 696 nM (s.e.m. 160, n=9) and 727 nM (s.e.m. 121, n=5) respectively. After 1 μM thapsigargin, 100 nM ET-1 had no effect on [Ca2+]i Oscillations in [Ca2+]i were frequently observed following 100 nM ET-1. In Ca2+-free extracellular solution, mean resting [Ca2+]i was reduced by 37 nM (s.e.m. 5, n=11) and the mean transient increase in [Ca2+]i in response to ET-1 was 419 nM (s.e.m. 97, n=5). Inhibition of the plasma membrane Ca-ATPase with La3+ halved the rate of [Ca2+]i removal from the cytoplasm following ET-1. The PKC inhibitor, chelerythrine (1 μM), reduced the ET-1 induced increase in [Ca2+]i to 349 nM (s.e.m. 97, n=5) and also reduced the rate of removal of [Ca2+]i Ligand binding studies demonstrated ETA receptor expression in MDCK cells sensitive to ET-1. Conclusions. ET-1 releases Ca2+ from IP3-sensitive stores in MDCK cells as well as stimulating extracellular Ca2+ entry leading to oscillations of [Ca2+]i. Ca2+ responses to ET-1 are potentiated by PKC; the plasma membrane Ca ATPase contributes to removal of Ca2+ from the cytoplasm.</div></front></TEI><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Angleterre</li><li>Grand Londres</li></region><settlement><li>Londres</li></settlement></list><tree><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Parkinson, N A" sort="Parkinson, N A" uniqKey="Parkinson N" first="N. A." last="Parkinson">N. A. Parkinson</name></region><name sortKey="Hendry, B M" sort="Hendry, B M" uniqKey="Hendry B" first="B. M." last="Hendry">B. M. Hendry</name><name sortKey="James, A F" sort="James, A F" uniqKey="James A" first="A. F." last="James">A. F. James</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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