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dc.contributor.authorMoore, Edwin D. W.
dc.contributor.authorFay, Fredric S.
dc.date2022-08-11T08:09:36.000
dc.date.accessioned2022-08-23T16:37:18Z
dc.date.available2022-08-23T16:37:18Z
dc.date.issued1993-09-01
dc.date.submitted2009-04-02
dc.identifier.citation<p>Proc Natl Acad Sci U S A. 1993 Sep 1;90(17):8058-62.</p>
dc.identifier.issn0027-8424 (Print)
dc.identifier.pmid8367463
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38986
dc.description.abstractbeta-Agonists cause an inhibition of contractility and a transient stimulation of Na+/K+ pumping in smooth muscle cells of the stomach from the toad Bufo marinus. To determine if the stimulation of Na+/K+ pumping causes changes in intracellular [Na+] ([Na+]i) that might link Na+ pump stimulation to decrease Ca2+ availability for contraction, [Na+]i was measured in these cells with SBFI, a Na(+)-sensitive fluorescent indicator. Basal [Na+]i was 12.8 +/- 4.2 mM (n = 32) and was uniform throughout the cell. In response to isoproterenol, [Na+]i decreased an average of 7.1 +/- 1.1 mM in 3 sec. Since this decrease in [Na+]i could be completely blocked by inhibition of the Na+ pump, or by blockade of the beta-receptor, [Na+]i reduction is the result of occupation of the beta-receptor by isoproterenol and subsequent stimulation of the Na+ pump. 8-Bromoadenosine 3',5'-cyclic monophosphate and forskolin mimicked the effect of isoproterenol, indicating that the sequence of events linking beta-receptor occupation to Na+ pump stimulation most likely includes activation of adenylate cyclase, production of cAMP, and stimulation of cAMP-dependent protein kinase. The decrease in [Na+]i is sufficiently large and fast that it is expected to stimulate turnover of the Na+/Ca2+ exchanger in the Ca2+ extrusion mode, thereby accounting for the observed linkage between stimulation of the Na+/K+ pump and inhibition of contractility in response to beta-adrenergic agonists.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=8367463&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC47287/
dc.subject8-Bromo Cyclic Adenosine Monophosphate
dc.subjectAnimals
dc.subjectBenzofurans
dc.subjectBufo marinus
dc.subjectCarbachol
dc.subjectEthers, Cyclic
dc.subjectFluorescent Dyes
dc.subjectForskolin
dc.subjectIsoproterenol
dc.subjectKinetics
dc.subjectMicroscopy, Fluorescence
dc.subjectMuscle, Smooth
dc.subjectOuabain
dc.subjectPindolol
dc.subjectPotassium
dc.subjectSodium
dc.subjectStomach
dc.subjectTime Factors
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleIsoproterenol stimulates rapid extrusion of sodium from isolated smooth muscle cells
dc.typeJournal Article
dc.source.journaltitleProceedings of the National Academy of Sciences of the United States of America
dc.source.volume90
dc.source.issue17
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/1813
dc.identifier.contextkey808579
html.description.abstract<p>beta-Agonists cause an inhibition of contractility and a transient stimulation of Na+/K+ pumping in smooth muscle cells of the stomach from the toad Bufo marinus. To determine if the stimulation of Na+/K+ pumping causes changes in intracellular [Na+] ([Na+]i) that might link Na+ pump stimulation to decrease Ca2+ availability for contraction, [Na+]i was measured in these cells with SBFI, a Na(+)-sensitive fluorescent indicator. Basal [Na+]i was 12.8 +/- 4.2 mM (n = 32) and was uniform throughout the cell. In response to isoproterenol, [Na+]i decreased an average of 7.1 +/- 1.1 mM in 3 sec. Since this decrease in [Na+]i could be completely blocked by inhibition of the Na+ pump, or by blockade of the beta-receptor, [Na+]i reduction is the result of occupation of the beta-receptor by isoproterenol and subsequent stimulation of the Na+ pump. 8-Bromoadenosine 3',5'-cyclic monophosphate and forskolin mimicked the effect of isoproterenol, indicating that the sequence of events linking beta-receptor occupation to Na+ pump stimulation most likely includes activation of adenylate cyclase, production of cAMP, and stimulation of cAMP-dependent protein kinase. The decrease in [Na+]i is sufficiently large and fast that it is expected to stimulate turnover of the Na+/Ca2+ exchanger in the Ca2+ extrusion mode, thereby accounting for the observed linkage between stimulation of the Na+/K+ pump and inhibition of contractility in response to beta-adrenergic agonists.</p>
dc.identifier.submissionpathoapubs/1813
dc.contributor.departmentDepartment of Physiology
dc.source.pages8058-62


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