In the sinus node of PAH rats, there was a significant downregulation of many ion channels and Ca2+-handling genes that could explain the dysfunction: HCN1 and HCN4 (responsible for pacemaker current, If), Cav1.2, Cav1.3 and Cav3.1 (responsible for L- and T-type Ca2+ currents, ICa,L and ICa,T), NCX1 (responsible for Na+–Ca2+ exchanger) and SERCA2 and RYR2 (Ca2+-handling molecules). This evidence concerns the gene CACNA1C and pulmonary arterial hypertension.