Regional distribution of ?1- and ?2-adrenoceptors in the failing and nonfailing human heart

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Abstract
Total β-adrenoceptor density and β1- and β2-subtype distribution in right and left atria and in different ventricular regions from 14 failing and seven nonfailing human hearts have been compared. End-stage heart failure was due to idiopathic dilated cardiomyopathy (n=8) or ischaemic cardiomyopathy (n=6). In nonfailing hearts the total β-adrenoceptor density was similar in the right and left atria and in all the ventricular regions studied (about 70 to 80 fmol/mg protein). The β1:β2-adrenoceptor ratio in both nonfailing atria was similar (about 70:30%) and was significantly smaller than in the different regions of both ventricles (about 80:20%). The β1-subtype density was similar in nonfailing atria and ventricles (about 55 fmol/mg protein). The β2-subtype density was significantly higher in the right and left atrium (about 25 fmol/mg protein) than in both ventricles (about 15 fmol/mg protein). In patients with end-stage heart failure due to idiopathic dilated cardiomyopathy or ischaemic cardiomyopathy the total β-adrenoceptor density was reduced by 50–60% in all regions. On the other hand, the β1- and β2-subtype distribution differed with the cause of heart failure. In patients with idiopathic dilated cardiomyopathy, the β1-adrenoceptor density was lower in all regions, but the β2-adrenoceptor density was not significantly reduced. In patients with ischaemic cardiomyopathy both β1- and β2-adrenoceptors were reduced in all regions. It is concluded that downregulation of β-adrenoceptors in patients with end-stage idiopathic dilated cardiomyopathy or ischaemic cardiomyopathy occurs uniformly throughout the heart. The results support the hypothesis that changes in β-adrenoceptor subtypes may be related to the cause of heart failure.

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