Enhanced β-adrenergic cardiac reserve in Trpm4−/− mice with ischaemic heart failure

Heart failure (HF) is a complex syndrome characterized by critically reduced cardiac contractility and function. We have shown previously that Transient Receptor Potential Melastatin 4 protein (TRPM4) functions as a Ca(2+)-activated non-selective cation channel and constitutes a novel regulator of ventricular contractility. In healthy Trpm4-deficient (Trpm4(-/-)) mice, we observed increased cardiac contractile function after β-adrenergic stimulation. In the current study, cardiac performance was examined in wild-type (WT) and Trpm4(-/-) mice with severe ischaemic HF.