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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Membrane proteins of the myocytes in cardiac overload.

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 beta-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 beta-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 beta-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 beta-adrenergic and muscarinic receptors present on the hypertrophied myocytes suggests a non-regulation for the genes coding for these receptors.[1]


  1. Membrane proteins of the myocytes in cardiac overload. Mansier, P., Chevalier, B., Mayoux, E., Charlemagne, D., Ollivier, L., Callens-el Amrani, F., Swynghedauw, B. British journal of clinical pharmacology. (1990) [Pubmed]
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