Cardiac dysfunction is the main cause of mortality and morbidity in the commonly occurring genetic disorder Autosomal Dominant Polycystic Kidney Disease (ADPKD). However, how the polycystins function in the heart, and how mutations in these proteins predispose ADPKD patients to cardiac disorders before development of renal dysfunction remains poorly studied. Here, we investigated the effect of decreased polycystin 2 (PC2) levels, a calcium channel that interacts with the ryanodine receptor, on cardiac function in mice of different ages. We examined 1 and 9 month old heterozygous PC2 mice (Pkd2+/-) to determine if decreased amounts of functional polycystin 2 leads to impaired cardiac function with aging. We observed changes in calcium handling proteins in 1 month old Pkd2+/- mice, and these changes were exacerbated in 9 month old Pkd2+/- mice. Anatomically, the 9 month old Pkd2+/- mice had thinner left ventricular walls, consistent with dilated cardiomyopathy, and the left ventricular ejection fraction was decreased, as assessed with M-mode echocardiography whilst under inhaled isoflurane anaesthesia. Intriguingly, in response to acute isoproterenol stimulation (0.03, 0.1 and 1 mg/kg/body weight) to examine β-adrenergic responses using M-mode echocardiography (whilst under inhaled isoflurane anaesthesia), the 9 month old Pkd2+/- mice exhibited a stronger contractile response, which also coincided with preserved localization of the β2 adrenergic receptor. Importantly, the Pkd2+/- mice did not have any renal impairment. We conclude that the cardiac-related impact of decreased polycystin 2 progresses over time towards cardiac dysfunction and altered adrenergic signaling. These results provide further evidence that polycystin 2 provides a critical function in the heart, independent of renal involvement.