Heart Adrenoceptor Gene Expression and Binding Sites in the Human Failing Heart

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Abstract
Adrenergic regulation of the heart function is well documented by many studies. Catecholamines act through α1‐, β1‐, β2‐, and β3‐adrenoceptors (ARs) in the heart. There are many findings about the changes of β1‐ and β2‐AR in heart failure (HF). On the other hand, the role of other AR subtypes is not clear yet. We focused on determining how HF could affect gene expression and specific ligand binding to α1A‐, α1B‐, α1D‐, β1‐, β2‐, and β3‐AR. Hearts from 11 patients with HF subjected to transplantation were investigated. As a control, corresponding parts from hearts not suitable for transplantation were used. We have found significantly higher mRNA levels of α1A‐, α1B‐,β1‐, and β2‐AR in the left ventricle of failing hearts compared to the levels in controls. β3‐AR mRNA levels in the left ventricle of failing hearts were not changed. No changes in mRNA levels of all receptors studied in other cardiac areas were found. On the other hand, binding studies showed a substantial decrease in left ventricles of failing hearts in all α1‐AR subtypes and in β1‐ and β2‐AR. However, the binding to β3‐AR was not changed. Our results suggest that α1‐AR changes might be part of a compensatory mechanism, by which the heart suffering from the HF tries to secure its function, and it could be hypothesized that ineffective β3‐AR regulation might be involved in development of HF. According to our knowledge, this is the first report about the β3‐AR binding in HF.

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