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. 1990;30(Suppl 1):43S–48S. doi: 10.1111/j.1365-2125.1990.tb05467.x

Membrane proteins of the myocytes in cardiac overload

Pascal Mansier, Brigitte Chevalier, Eric Mayoux, Danièle Charlemagne, Laurence Ollivier, Francine Callens-el Amrani, Bernard Swynghedauw
PMCID: PMC1368097  PMID: 2176528

Abstract

1 Hypertrophy of the cardiac myocytes resulting from a mechanical overload may be responsible for major membraneous modifications, either at the sarcolemmal or at the sarcoplasmic level. In this study several sarcolemmal markers such as β-adrenoceptors, muscarinic receptors or (Na+,K+)-ATPase were investigated in an experimental model of cardiac hypertrophy, the chronic aortic stenosis in adult rats.

2 Left ventricular β-adrenoceptor density (expressed in fmol mg-1 protein) was decreased in the aortic stenosis group by about 30%; however, when expressed in number of receptors per cardiac cell β-adrenoceptor number in the hypertrophied myocytes was unchanged.

3 Similarly, the number of muscarinic receptors in the hypertrophied cells, expressed as number of receptors per cardiac cell, was unchanged.

4 The number of (Na+,K+)-ATPase molecules with high affinity for ouabain was markedly increased in the hypertrophied myocytes, while those with low affinity for ouabain were not.

5 These results indicate the necessity in chronic hypertrophy to calculate receptors not only in density (fmol mg-1 protein) but also in number per cardiac cell. The unchanged number of β-adrenergic and muscarinic receptors present on the hypertrophied myocytes suggests a non-regulation for the genes coding for these receptors.

Keywords: β-adrenoceptors; muscarinic receptors; (Na+,K+)-ATPase; sarcoplasmic reticulum; cardiac hypertrophy; cardiac insufficiency

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Selected References

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