Abstract:
:Exposure of fine trabeculae isolated from the ferret right ventricle to media depleted of Ca2+, with a rapid perfusion system, causes a depolarization of the membrane and a rise in aiNa. This rise in aiNa is sigmoidally dependent upon the bathing free [Ca2+], is antagonized by reduction of the [Na]o, raised [Mg]o and PN200-110 but augmented by removal of Mg2+ or inhibition of the Na-pump. On repletion of Ca2+, the strength of the resulting contracture depends upon the transmembrane. Na-gradient at the moment of Ca-repletion. The effects of reduced [Na]o, during Ca-depletion, depend upon the cation used with replacement by Li much greater than choline greater than tetramethylammonium. These are determined by the change in the transmembrane gradient for Na+ and any additional action the replacing ion has upon the Ca-channels, the Na-pump and the Na/Ca exchange. The effects described are consistent with the hypothesis that the intensity of the calcium paradox in mammalian ventricle is primarily determined by the entry of Na+ through L-type Ca-channels during the period of Ca-depletion and the Ca-loading on Ca-repletion due to the effect of the raised aiNa upon the Na/Ca exchange.
journal_name
J Mol Cell Cardioljournal_title
Journal of molecular and cellular cardiologyauthors
Bhojani IH,Chapman RAdoi
10.1016/0022-2828(90)90953-ysubject
Has Abstractpub_date
1990-05-01 00:00:00pages
507-22issue
5eissn
0022-2828issn
1095-8584pii
0022-2828(90)90953-Yjournal_volume
22pub_type
杂志文章abstract:BACKGROUND:Hypertrophic cardiomyopathy (HCM) is a prevalent and complex cardiovascular condition. Despite being strongly associated with genetic alterations, wide variation of disease penetrance, expressivity and hallmarks of progression complicate treatment. We aimed to characterize different human isogenic cellular m...
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
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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
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章,评审
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章,评审
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
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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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更新日期:1994-05-01 00:00:00
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journal_title:Journal of molecular and cellular cardiology
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更新日期:1989-04-01 00:00:00
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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
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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
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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
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
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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,评审
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
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journal_title:Journal of molecular and cellular cardiology
pub_type: 杂志文章
doi:10.1006/jmcc.1993.1046
更新日期:1993-04-01 00:00:00