Effect of captopril on myocardial β-adrenoceptor density and Giα-proteins in patients with mild to moderate heart failure due to dilated cardiomyopathy

In end-stage heart failure due to idiopathic dilated cardiomyopathy ß₁-adrenoceptors are downregulated and G_1a-proteins are upregulated. The aim of the present study was to investigate the influence of the angiotensin-converting enzyme inhibitor captopril on ß-adrenoceptor density and G_ia-proteins in sequential endomyocardial biopsies. Nineteen patients with mild to moderate congestive heart failure due to idiopathic dilated cardiomyopathy (NYHA Class II–III) were studied before and after 8–11 weeks of therapy. Patients were randomised into a captopril and a control group; 9 patients received captopril 12.5–50 mg per day, (divided in 2–3 doses) p.o. in addition to “conventional” therapy with digoxin and diuretics, and 10 controls received “conventional” therapy only. Echocardiography, spiroergometry, right heart catheterisation and endomyocardial biopsies were performed before (baseline) and after treatment. Compared to baseline, captopril increased total ß-adrenoceptor density by selectively increasing ß₁-adrenoceptors (31.6 vs 41.2 fmol·mg^-1; p<0.05) but had no significant effect on G_ia-proteins. The results indicate that treatment with angiotensin-converting enzyme inhibitors partly restores myocardial ß₁-adrenoceptor density, and this action effect may contribute to the clinical improvement of patients with idiopathic dilated cardiomyopathy treated in this way.