Acceleration of contraction by beta-adrenoceptor stimulation is greater in ventricular myocytes from failing than non-failing human hearts.

Myocytes from failing human ventricle contract and relax more slowly than those from non-failing. This has been suggested to result from the lowering of basal cyclic AMP level in failing myocardium, and the consequent withdrawal of a tonic lusitropic effect. We present data to support this hypothesis by demonstrating that the acceleration of contraction and relaxation by beta-adrenoceptor stimulation is greater in myocytes from failing than non-failing heart. This is despite the desensitisation of the inotropic effect of isoprenaline in the same failing cells. Following beta-adrenoceptor stimulation, speeds of contraction and relaxation are normalised in myocytes from failing heart, with final values not significantly different from non-failing.