Augmented Cardiac Inotropy by Phosphodiesterase Inhibition Requires Phosphorylation of Rad and Increased Calcium Current.

This research letter, published in the journal Circulation, explores the effects of phosphodiesterase (PDE) inhibitors on cardiac contractility. The study reveals that PDE inhibitors enhance intrinsic cardiomyocyte contractility and arterial dilation, resulting in increased cardiac output and reduced workload on the heart. The researchers also discovered that the phosphorylation of a protein called Rad is necessary for the augmentation of cardiac contractility by PDE inhibitors, leading to increased calcium influx and cardiomyocyte contraction. These findings have potential implications for the development of targeted therapeutics for heart failure. [Extracted from the article]