[Background] Voltage dependent Ca²⁺ channels are divided to L-, T-, N-, P/Q-, and R- types, and N-type Ca²⁺ channel (NCC) are mainly expressed in nerve terminal. Recently, NCC has been reported to express in adrenal gland and renal tubular cells. We examined whether NCC is expressed in cardiac myocytes and if so, the roles of this channel. [Methods and Results] NCC mRNA and protein are expressed in neonatal rat cardiac myocytes, using real time PCR and Western blot analysis. Immunocytochemistry showed this channel was expressed on myocyte plasma membrane. After birth the expression level of this channel in cardiac tissue was gradually decreased within 2 weeks. In pathological condition, such as 5 hours of hypoxia followed by 30 minutes of reoxygenation (H/R) and norepinephrine (10^-5 mol/L, 24 hours) increased NCC expression in neonatal cultured myocytes. In addition, in adult rats (12 weeks) mRNA level of this channel was also increased in non-infarcted myocardium after 4 weeks of myocardial infarction. Furthermore, to clarify the role of NCC in myocyte, we examine the effect of ω-conotoxin, a selective NCC blocker. ω-conotoxin significantly suppressed H/R- and norepinephrine-induced lethal myocytes injury, assessed by LDH activity in cultured medium and caspase 3 activity in myocytes. [Conclusion] NCC is expressed in neonatal and pathological cardiac tissue, and augmented myocyte lethal injury.