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dc.contributor.authorGaur, Shikha
dc.contributor.authorYamaguchi, Hiroshi
dc.contributor.authorGoodman, H. Maurice
dc.date2022-08-11T08:10:02.000
dc.date.accessioned2022-08-23T16:52:51Z
dc.date.available2022-08-23T16:52:51Z
dc.date.issued2000-01-29
dc.date.submitted2008-07-09
dc.identifier.citation<p>Endocrinology. 2000 Feb;141(2):513-9.</p>
dc.identifier.issn0013-7227 (Print)
dc.identifier.pmid10650930
dc.identifier.urihttp://hdl.handle.net/20.500.14038/42141
dc.description.abstractGH promptly increases cytosolic free calcium ([Ca2+]i) in freshly isolated rat adipocytes. Adipocytes deprived of GH for 3 h or longer are incapable of increasing [Ca2+]i in response to GH, but instead respond in an insulin-like manner. Insulin blocks the GH-induced increase in [Ca2+]i in GH-replete cells and stimulates the sodium pump (i.e. Na+/K+-ATPase), thereby hyperpolarizing the cell membrane. Blockade of the Na+/K+-ATPase with 100 microM ouabain reversed these effects of insulin and enabled GH to increase [Ca2+]i in GH-deprived adipocytes. Both insulin and GH activated the sodium pump in GH-deprived adipocytes, as indicated by increased uptake of 86Rb+. Decreasing availability of intracellular Na+ by blockade of Na+/K+/ 2Cl- symporters or Na+/H+ antiporters abolished the effects of both hormones on 86Rb+ uptake and enabled both GH and insulin to increase [Ca2+]i in GH-deprived adipocytes. The data suggest that hormonal stimulation of Na+/K+-ATPase activity interferes with activation of voltage-sensitive calcium channels by either membrane hyperpolarization or some unknown interaction between the sodium pump and calcium channels.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=10650930&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1210/en.141.2.513
dc.subjectAdipocytes
dc.subjectAnimals
dc.subjectBiological Transport
dc.subjectBumetanide
dc.subjectCalcium
dc.subjectCells, Cultured
dc.subjectCytosol
dc.subjectEnzyme Activation
dc.subjectGrowth Hormone
dc.subjectInsulin
dc.subjectKinetics
dc.subjectMale
dc.subjectModels, Biological
dc.subjectNimodipine
dc.subjectOuabain
dc.subjectRats
dc.subjectRubidium
dc.subjectSodium-Potassium-Exchanging ATPase
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleActivation of the sodium pump blocks the growth hormone-induced increase in cytosolic free calcium in rat adipocytes
dc.typeJournal Article
dc.source.journaltitleEndocrinology
dc.source.volume141
dc.source.issue2
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/515
dc.identifier.contextkey544997
html.description.abstract<p>GH promptly increases cytosolic free calcium ([Ca2+]i) in freshly isolated rat adipocytes. Adipocytes deprived of GH for 3 h or longer are incapable of increasing [Ca2+]i in response to GH, but instead respond in an insulin-like manner. Insulin blocks the GH-induced increase in [Ca2+]i in GH-replete cells and stimulates the sodium pump (i.e. Na+/K+-ATPase), thereby hyperpolarizing the cell membrane. Blockade of the Na+/K+-ATPase with 100 microM ouabain reversed these effects of insulin and enabled GH to increase [Ca2+]i in GH-deprived adipocytes. Both insulin and GH activated the sodium pump in GH-deprived adipocytes, as indicated by increased uptake of 86Rb+. Decreasing availability of intracellular Na+ by blockade of Na+/K+/ 2Cl- symporters or Na+/H+ antiporters abolished the effects of both hormones on 86Rb+ uptake and enabled both GH and insulin to increase [Ca2+]i in GH-deprived adipocytes. The data suggest that hormonal stimulation of Na+/K+-ATPase activity interferes with activation of voltage-sensitive calcium channels by either membrane hyperpolarization or some unknown interaction between the sodium pump and calcium channels.</p>
dc.identifier.submissionpathoapubs/515
dc.contributor.departmentDepartment of Physiology
dc.source.pages513-9


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