Dendroaspis natriuretic peptide (DNP), a new member of the natriuretic peptide family, is structurally similar to atrial, brain, and C-type natriuretic peptides. However, the effects of DNP on the cardiac function are poorly defined. In the present study, we examined the effect of DNP on the cardiac L-type $Ca^{2+}$ channels in rabbit ventricular myocytes. DNP inhibited the L-type $Ca^{2+}$ current ($I_{Ca,L}$) in a concentration dependent manner with a $IC_{50}$ of 25.5 nM, which was blocked by an inhibitor of protein kinase G (PKG), KT5823 (1 ${mu}M$). DNP did not affect the voltage dependence of activation and inactivation of $I_{Ca,L}$. The ${alpha}_{1c}$ subunit of cardiac L-type $Ca^{2+}$ channel proteins was phosphorylated by the treatment of DNP (1 ${mu}M$), which was completely blocked by KT5823 (1 ${mu}M$). Finally, DNP also caused the shortening of action potential duration in rabbit ventricular tissue by $22.3{pm}4.2%$ of the control (n = 6), which was completely blocked by KT5823 (1 ${mu}M$). These results clearly indicate that DNP inhibits the L-type $Ca^{2+}$ channel activity by phosphorylating the $Ca^{2+}$ channel protein via PKG activation.