Cardiovascular disease is the biggest worldwide killer - it affects more than 7 million people in the UK alone, with hypertension being the most important risk factor for the development of heart failure. A particular branch of cardiovascular disease - cardiac conduction system dysfunction - remains poorly understood. Sinus node dysfunction is a pathology observed in the elderly, heart failure, myocardial infarction and athletes. In heart failure, sinus node dysfunction and bradyarrhythmic deaths are common. Therefore, it is of importance to identify key proteins involved in the biogenesis and development of sinus node disease. Calcium/calmodulin - dependent protein kinase II (CaMKII) is a kinase involved in normal cardiac function and plays a crucial role in pacemaking in the heart. However, CaMKII is also implicated in cardiac pathologies - it has involvement in arrhythmias, hypertrophy, cardiomyopathies and heart failure. In addition, when trapped in its constitutively activate state, CaMKII promotes sinus node dysfunction. The main aim of this study was to investigate the effect of CaMKII on hypertension and sinus node function (in particular, ion channel expression) in hypertensive heart disease. A second aim was to investigate the effect of CaMKII on sinus node bradycardia in athletic training. To address the aims, two animal models were used - an angiotensin II (ANGII)-induced hypertensive heart disease model and a swimming model of athletic training. In addition, the study incorporated AC3-I mice - genetically modified animals that have reduced CaMKII activity in the heart. In the hypertensive model, ANGII promoted 35% increase in systolic (from 119 mmHg to 160 mmHg) and 30% increase in diastolic (from 92 mmHg to 120 mmHg) blood pressure in wild type ANGII-treated animals. This increase in blood pressure was halved by CaMKII inhibition in AC3-I mice - systolic blood pressure was increased by only 15% (from 117 mmHg to 135 mmHg) and diastolic blood pressure was increased by only 17% (from 90 mmHg to 105 mmHg). The heart rate in the conscious mouse was unchanged in ANGII-treated animals (both wild type and AC3-I). However, the intrinsic heart rate measured in ex vivo sinus node preparations was decreased in wild type ANGII-treated animals (bradycardia of 17%). In the sinus node of wild type ANGII-treated animals, there was a significant downregulation in the mRNA level of two Ca2+ channels, Cav1.2 and Cav1.3, and this could be involved in the bradycardia. In AC3-I ANGII-treated animals, there was no downregulation of the Ca2+ channels and no bradycardia. In addition, oxidised CaMKII was increased in the sinus node of wild type ANGII-treated animals and not in the AC3-I mice indicating a positive benefit of CaMKII inhibition by AC3-I. In the animal model of athletic training, wild type mice developed bradycardia after three weeks of swimming. This response was reduced in AC3-I animals which suggests an involvement of CaMKII in the development of the sinus bradycardia. In conclusion, this study shows that ANGII produces hypertension and sinus node dysfunction accompanied by ion channel remodelling in the sinus node. Heart-specific inhibition of CaMKII reduces the hypertension and exerts a protective effect on the sinus node: it prevents the bradycardia and Ca2+ channel remodelling seen in ANGII-induced hypertension. This study shows a link between hypertension and sinus node function and a role for CaMKII in this.