Abstract:
:In mammalian myocardium, muscle contraction is regulated by the rapid release of Ca2+ ions through ryanodine-sensitive Ca2+ release channels present in the intracellular membrane compartment, sarcoplasmic reticulum (SR). In this study, the effects of regional ischemia on intrinsic SR Ca2+ release channel function were determined by studying the Ca2+ transport and release, and [3H]ryanodine binding properties of whole muscle homogenates and SR-enriched membrane fractions from normal and ischemic myocardium. Measurement of oxalate-supported 45Ca(2+)-uptake rates before and after pretreatment with 1 mM ryanodine, indicated that the SR Ca2+ release channel retained its ability to be effectively closed by the channel-specific probe ryanodine after 15 and 60 min of ischemia. 45Ca2+ efflux from, and high-affinity [3H]ryanodine binding to SR-enriched vesicle fractions indicated retention of regulation of Ca2+ release channel activity by Ca2+, Mg2+ and adenine nucleotide in 15 and 60 min ischemic samples. Further, sodium dodecylsulfate polyacrylamide gel and immunoblot analysis revealed no proteolytic degradation of the M(r) 565,000 SR Ca2+ release channel polypeptide after 15 and 60 min of ischemia. These results suggested a minimal, if any, loss of intrinsic SR Ca2+ release channel function in ischemic hearts.
journal_name
J Mol Cell Cardioljournal_title
Journal of molecular and cellular cardiologyauthors
Darling EM,Lai FA,Meissner Gdoi
10.1016/0022-2828(92)93181-ikeywords:
subject
Has Abstractpub_date
1992-10-01 00:00:00pages
1179-88issue
10eissn
0022-2828issn
1095-8584pii
0022-2828(92)93181-Ijournal_volume
24pub_type
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journal_title:Journal of molecular and cellular cardiology
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journal_title:Journal of molecular and cellular cardiology
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
doi:10.1006/jmcc.1998.0905
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章,评审
doi:10.1016/j.yjmcc.2010.08.005
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journal_title:Journal of molecular and cellular cardiology
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doi:10.1006/jmcc.1998.0794
更新日期:1998-11-01 00:00:00
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doi:10.1016/0022-2828(89)90607-x
更新日期:1989-07-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
doi:10.1016/j.yjmcc.2007.12.008
更新日期:2008-03-01 00:00:00
abstract::Cardiovascular diseases (CVDs) and renal impairment interact in a complex and interdependent manner, which makes clarification of possible pathogenesis between CVDs and renal diseases very challenging and important. There is increasing evidence showing that both asymmetric dimethylarginine (ADMA) and symmetric dimethy...
journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章,评审
doi:10.1016/j.yjmcc.2017.09.010
更新日期:2017-12-01 00:00:00
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更新日期:1995-01-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
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更新日期:1998-07-01 00:00:00
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更新日期:2001-08-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
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更新日期:1986-06-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
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abstract::The failure of adenosine receptor antagonists to consistently attenuate metabolic coronary vasodilation suggests that adenosine is not a primary regulator of functional hyperemia. An alternative hypothesis, however, is that metabolic stimulation of the heart in the presence of an adenosine receptor antagonist results ...
journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
doi:10.1016/0022-2828(91)90132-6
更新日期:1991-08-01 00:00:00
abstract:INTRODUCTION:Fibroblast activation protein α (FAP) is a membrane-bound serine protease expressed by activated fibroblasts during wound healing in the skin. Expression of FAP after myocardial infarction (MI) and potential effects on cardiac wound healing are largely unknown. METHODS:MI was induced in rats and FAP expre...
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pub_type: 杂志文章
doi:10.1016/j.yjmcc.2015.08.016
更新日期:2015-10-01 00:00:00