Drug- and disease-induced changes of human cardiac 1- and 2-adrenoceptors

Publisher Website
Google Scholar
Abstract
Cardiac β-adrenoceptor density and subtype distribution has been determined in different kinds of heart failure. A decrease in cardiac β-adrenoceptor function appears to be a general phenomenon in all kinds of heart failure. However, cardiac β1 and β2-adrenoceptors seem to be differentially affected in different kinds of heart failure: while in end-stage idiopathic dilated cardiomyopathy the diminished cardiac β-adrenoceptor function is due to a selective loss in β1-adrenoceptors, in mitral valve disease, tetralogy of Fallot and end-stage ischaemic cardiomyopathy it is characterized by a concomitant reduction in β1- and β2-adrenoceptors. Chronic treatment of heart failure patients with β-adrenoceptor antagonists leads to an up-regulation of cardiac β-adrenoceptors, but in a subtype-selective fashion: β1-selective antagonists increase only cardiac β1-adrenoceptors, whereas non-selective antagonists increase both β1- and β2-adrenoceptors. Such a (subtype-selective) ‘recovery’ of cardiac β-adrenoceptors may be one reason for the beneficial effects of low-dose β-adrenoceptor antagonist treatment in patients with severe heart failure.

This publication has 0 references indexed in Scilit: