Altered expression of α-subunits of G proteins in failing human hearts

Feldman, Arthur M.; Cates, A. E.; Bristow, Michael R.; Dop, Cornelis Van

doi:10.1016/0022-2828(89)90646-9

Cited by 79 publications

(9 citation statements)

References 21 publications

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“…Studies are in progress in our laboratory to quantify mRNA to test this hypothesis. This apparent non response is in contrast to the increased level of mRNA obtained for Gi in a human heart failure (Feldman et al, 1988(Feldman et al, , 1989.…”

Section: Discussioncontrasting

confidence: 56%

Membrane proteins of the myocytes in cardiac overload.

Mansier

Chevalier

Mayoux

et al. 1990

Brit J Clinical Pharma

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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 ,-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 13-adrenoceptor density (expressed in fmol mg-' protein) was decreased in the aortic stenosis group by about 30%; however, when expressed in number of receptors per cardiac cell ,-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-' protein) but also in number per cardiac cell. The unchanged number of ,-adrenergic and muscarinic receptors present on the hypertrophied myocytes suggests a non-regulation for the genes coding for these receptors.

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Section: Discussioncontrasting

confidence: 56%

Membrane proteins of the myocytes in cardiac overload.

Mansier

Chevalier

Mayoux

et al. 1990

Brit J Clinical Pharma

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“…One group described G;a,3 to be the predominant G;a-subtype in human ventricular myocardium and found no increase in the immunodetectable level of any G;a subtypes (Feldman et al 1991a). In an earlier publication, the same group demonstrated increases in G;a,3-and G,a-mRNA levels in heart failure (Feldman et al 1989). In a more recent study, using quantitative PCR, the previous data were reappraised, and G'~3 or G",-mRNA levels were reported to be unchanged (Feldman et al 1991b).…”

Section: Human Heart Failurementioning

confidence: 95%

G proteins and the heart

Eschenhagen

1993

Cell Biology International

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“…This impairment of presynaptic sympathetic reuptake is a probable reason for increased local exposure of the failing heart to norepinephrine. In experimental models, excess catecholamine stimulation has been shown to be associated with alterations in adrenergic signal transduction, resulting in reduced diastolic and systolic contractile function [7,8] . Furthermore, direct toxicity of norepinephrine to myocytes has been demonstrated [9] .…”

Section: Introductionmentioning

confidence: 99%