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European Heart Journal 1994 15(Supplement D):30-34; doi:10.1093/eurheartj/15.suppl_D.30
Copyright © 1994 by the European Society of Cardiology.
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© 1994 The European Society of Cardiology

Quantification of β-Adrenoceptors and β-Adrenoceptor Kinase on Protein and mRNA Levels in Heart Failure

M. Böhm*, and M. J. Lohse{dagger}

* Klinik III für Innere Medizin der Universität zu Köln Köln, Germany
{dagger} Laboratorium für Molekulare Biologie der Universität München Germany

Correspondence: PD Dr M. Böhm, Klinik III für Innere Medizin der Universität zu Köln. Joseph-Stelzmann-Str. 9,50924 Köln, Germany

The alterations of the β-adrenoceptor adenylyl cyclase are reviewed. In failing myocardium, the down-regulation of β1adrenoceptors is accompanied by a decrease in steady state mRNA levels, as studied with quantitative polymerase chain reactions in dilated and ischaemic cardiomyopathy. The density of β2-adrenoceptors and β2-adrenoceptor mRNA was unchanged in both pathological conditions compared to non-failing myocardium. In addition to down-regulation of β1-receptor protein and mRNA, an increased activity of the β-adrenoceptor kinase (p-ARK) was observed. Correspondingly, quantification of P-ARK mRNA by a 5' and a middle portion PCR-product suggests that increased enzyme activity could be due to increased transcription. In summary, decreased steady state levels of β1-adrenoceptor mRNA could contribute to reduced β-adrenoceptor density in failing myocardium. The known uncoupling of β-adrenoceptors could be due to an increased mRNA expression and activity of β-ARK.

Key Words: Human myocardium • heart failure • β-adrenoceptors • G-proteins • β-adrenoceptor kinase • polymerase chain reaction


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