The membrane proteins of the overloaded and senescent heart.

Abstract:

:Cardiac hypertrophy which occurs during chronic mechanical overload is one of the numerous examples of biological adaptation to environmental requirements. As such, it is obtained at random by trial and error, and adaptation represents the sum of various modifications in gene expression, including the shift in isoform of myosin or in iso Na+, K+ ATPase, the decrease in beta-adrenergic and muscarinic receptors, ryanodine channels or SR Ca2+ ATPase densities and the unchanged density in Ca2+ current. Some of these changes are beneficial at the cellular level, but are finally detrimental for the organism as a whole, as is the slowing of Vmax. It was suggested that the calcium homeostasis of the hypertrophied cardiocyte was fragile and that this modified cell was less able to buffer the changes in the intracellular calcium, thus providing a biological basis for the arrhythmogenicity of the hypertrophied heart. These various modifications may provide a new key for future pharmaceutical research.

journal_name

Basic Res Cardiol

authors

Chevalier B,Charlemagne D,Callens-el Amrani F,Carre F,Moalic JM,Delcayre C,Mansier P,Swynghedauw B

doi

10.1007/978-3-642-72474-9_15

keywords:

subject

Has Abstract

pub_date

1992-01-01 00:00:00

pages

187-97

eissn

0300-8428

issn

1435-1803

journal_volume

87 Suppl 1

pub_type

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