Abstract
Nitric oxide (NO) is a gaseous signalling molecule that regulates cardiac function by targeting calcium handling protein kinases such as calcium/ calmodulin-dependent protein kinase II delta (CaMKIIδ). NO can alter CaMKIIδ activity in the heart and this leads to irregular heart rhythm (arrhythmias). Currently, it is unknown how the duration of NO exposure can affect cardiac function in the presence and absence of CaMKIIδ. This study was designed to determine how acute and chronic NO treatment affects cardiac arrhythmias in mice lacking CaMKIIδ.