Abstract:
:A plasma membrane preparation purified from guinea pig ventricles without the use of high concentrations of detergents or structure-disrupting salts was used to compare the mechanisms of controlling sodium, potassium-activated adenosinetriphosphatase (Na, K-ATPase) and adenylate cyclase activities. The basal ATPase activity of 4-6 mu moles P1/hour mg-1 protein, measured in 120 mM NaC1 or KC1, was approximately doubled in 100 mM NaC1 plus 20 mM KC1. This increment, the Na, K-ATPase, was abolished by 10-5M ouabain, the K1 for ouabain being approximately 3 X 10-7M. 1-Epinephrine had no effect on Na, K-ATPase, but NaF was inhibitory. Adenylate cyclase, which had a basal activity of approximately 50% by NaC1 or KC1 alone at concentrations up to 0.2M. There was no additional stimulation of adenylate cyclase activity when na+ K+ included together. Both 1-epinephrine and NaF cause significant stimulation of adenylate cyclase, but neither basal nor activated cyclic AMP PRODUCTION WAS INFLUENCED BY OUABAIN. Half-maximal stimulation was seen at approximately 5 X 10-6M 1-epinephrine. Both the catecholamine and NaF increased the V-max ofcardiac plasma membrane adenylate cyclase without significantly influencing Km. Increasing Ca2+ in the range between 10-7 and 10-3M inhibited basal, 1-epinephrine-stimulated, and NaF-stimulated activities. Basal rates of cyclic AMP production were more sensitive to Ca2+ than was 1-epinephrine stimulation was increased from approximately 60% in 0.5 mM EGTA to approximately 150% in 10-7M Ca2+ and 400% in 10-5M Ca2+. The inhibitory effect of Ca2+ on adenylate cyclase activity may represent a negative feed back mechanism by which elevation of intracellular Ca2+ concentration lowers cellular levels of cyclic AMP and thus reduces Ca2+ influx into the myocardium.
journal_name
Circ Resjournal_title
Circulation researchauthors
Tada M,Kirchberger MA,Iorio JM,Katz AMdoi
10.1161/01.res.36.1.8subject
Has Abstractpub_date
1975-01-01 00:00:00pages
8-17issue
1eissn
0009-7330issn
1524-4571journal_volume
36pub_type
杂志文章abstract::Therapy directed against the toxic effects of reactive oxygen species may reduce the final extent of ischemic injury in otherwise viable tissue irreversibly injured by the abrupt reoxygenation of reperfusion. In four groups of dogs, superoxide dismutase plus catalase (groups I-III) or saline (controls) (group IV) was ...
journal_title:Circulation research
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doi:10.1161/CIRCRESAHA.108.171736
更新日期:2008-04-11 00:00:00
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更新日期:1988-10-01 00:00:00
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更新日期:2014-06-20 00:00:00
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更新日期:2009-03-13 00:00:00
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pub_type: 杂志文章,评审
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更新日期:2002-08-23 00:00:00
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journal_title:Circulation research
pub_type: 杂志文章
doi:
更新日期:1977-05-01 00:00:00
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更新日期:1987-03-01 00:00:00
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pub_type: 杂志文章
doi:10.1161/01.res.83.9.916
更新日期:1998-11-02 00:00:00
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pub_type: 杂志文章
doi:10.1161/01.res.47.3.356
更新日期:1980-09-01 00:00:00
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更新日期:1998-04-06 00:00:00
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更新日期:2015-01-02 00:00:00
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更新日期:1977-06-01 00:00:00
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更新日期:2005-09-02 00:00:00
abstract:RATIONALE:Cardiac myocyte-specific deletion of either glycogen synthase kinase (GSK)-3α and GSK-3β leads to cardiac protection after myocardial infarction, suggesting that deletion of both isoforms may provide synergistic protection. This is an important consideration because of the fact that all GSK-3-targeted drugs, ...
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更新日期:2016-04-15 00:00:00
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更新日期:2001-06-22 00:00:00
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pub_type: 杂志文章,收录出版
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更新日期:1981-10-01 00:00:00
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journal_title:Circulation research
pub_type: 杂志文章
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更新日期:1995-10-01 00:00:00
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journal_title:Circulation research
pub_type: 杂志文章
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更新日期:1989-05-01 00:00:00
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更新日期:1996-09-01 00:00:00
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更新日期:2019-12-06 00:00:00
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pub_type: 杂志文章
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更新日期:1983-08-01 00:00:00