CaMKII signalling is reduced in the sinus node of a heart failure experimental model

Abstract

Heart failure (HF) is a complex syndrome in which sudden cardiac death is associated to pump failure, ventricular arrhythmias or severe bradycardias. Sinoatrial node (SAN) activity is regulated synergically by membrane ion currents (voltage-clock) and intracellular calcium handling (Ca2+-clock). Whereas SAN dysfunction has been associated with voltage-clock remodelling in HF patients, the Ca2+-clock remodelling in SAN remains to be elucidated. Here, we studied intracellular Ca2+ handling in SAN from a transverse aortic constriction (TAC) mouse model of HF.