Abstract:
:The positive inotropic effect of the beta-adrenoceptor agonist isoproterenol is accompanied by inhibition of phosphatase type 1 activity in myocardium. Indirect assays suggest that this effect is due to activation of protein phosphatase inhibitor-1, which inhibits phosphatase activity only when phosphorylated. To test this hypothesis directly, electrically stimulated (3 Hz) guinea pig ventricular preparations were perfused according to the Langendorff method with physiological buffers with or without 5 mCi 32P/heart, and then various concentrations of isoproterenol were applied. Contractility was recorded. Hearts were freeze-clamped and cAMP and inhibitor-1 activities were measured. In 32P-labeled hearts a protein at about 26 kd on autoradiograms of 12% sodium dodecyl sulfate gels was detected. Isoproterenol (1 microM) increased rate of tension development to 238% of the predrug value, cAMP concentrations 1.5-fold, and inhibitor-1 activity threefold. Concomitantly, there was an increase in a 32P-labeled band at about 26 kd from 380 to 540 pmol 32P/mg protein. This protein at about 26 kd, after transfer to nitrocellulose, was recognized by an antiserum prepared against rabbit skeletal muscle inhibitor-1. More radioactive protein of about 26 kd could be immunoprecipitated by the antiserum from isoproterenol-treated than from untreated hearts. It is concluded that a protein, probably identical to phosphatase inhibitor-1, is phosphorylated in vivo in the heart in the presence of isoproterenol. Phosphorylation of inhibitor-1 with consequent modification of type 1 phosphatase activity may contribute to the effects of isoproterenol in the heart.
journal_name
Circ Resjournal_title
Circulation researchauthors
Neumann J,Gupta RC,Schmitz W,Scholz H,Nairn AC,Watanabe AMdoi
10.1161/01.res.69.6.1450subject
Has Abstractpub_date
1991-12-01 00:00:00pages
1450-7issue
6eissn
0009-7330issn
1524-4571journal_volume
69pub_type
杂志文章abstract:RATIONALE:Slow nonuniform electric propagation in the border zone (BZ) of a healed myocardial infarct (MI) can give rise to reentrant arrhythmia. The extent to which this is influenced by structural rather than cellular electric remodeling is unclear. OBJECTIVE:To determine whether structural remodeling alone in the i...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/CIRCRESAHA.111.260943
更新日期:2012-07-20 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:2007-03-30 00:00:00
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更新日期:2007-04-13 00:00:00
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更新日期:1990-02-01 00:00:00
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更新日期:1986-04-01 00:00:00
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journal_title:Circulation research
pub_type: 杂志文章
doi:
更新日期:1980-06-01 00:00:00
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更新日期:1979-07-01 00:00:00
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pub_type: 杂志文章,评审
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更新日期:2016-02-05 00:00:00
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pub_type: 杂志文章
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更新日期:1981-08-01 00:00:00
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pub_type: 杂志文章
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更新日期:2006-11-24 00:00:00
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更新日期:1998-10-05 00:00:00
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pub_type: 杂志文章
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更新日期:1985-10-01 00:00:00
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pub_type: 杂志文章
doi:10.1161/01.res.87.3.201
更新日期:2000-08-04 00:00:00
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更新日期:2000-03-03 00:00:00
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pub_type: 杂志文章
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更新日期:2001-06-22 00:00:00
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doi:10.1161/CIRCRESAHA.109.195883
更新日期:2009-09-11 00:00:00
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更新日期:1990-07-01 00:00:00
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更新日期:1992-08-01 00:00:00
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pub_type: 杂志文章
doi:10.1161/01.res.78.3.504
更新日期:1996-03-01 00:00:00
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更新日期:2004-04-30 00:00:00
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更新日期:2008-09-26 00:00:00
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更新日期:2008-02-15 00:00:00
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更新日期:2008-10-10 00:00:00
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更新日期:1992-02-01 00:00:00
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更新日期:1992-01-01 00:00:00
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更新日期:1981-07-01 00:00:00
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更新日期:2013-08-30 00:00:00