Cardiac T-type Ca2+ channels are re-ex pressed in atrial and ventricular myocytes under various pathological conditions such as post-myocar dial infarction, hypertrophy and heart failure, but relatively little is known about the mechanisms.Our previous study found that bone morphogenetic pro tein-4(BMP4) was re-expressed in pathological car diac hypertrophy models and BMP4 mediated car diomyocyte hypertrophy.We hypothesized that BMP4 could up-regulate cardiac T-type Ca2+ channels in HL-1 atrial myocytes.The T-type Ca2+ currents were recorded by using patch-clamp technique and the expressions of Cav3.1 and Cav3.2 were measured by real-time PCR method in HL-1 cells.BMP4 and Cav3.1 mRNA expressions increased in the left atri um from the pressure-overload induced hypertrophy mice hearts.BMP4 treatment for 48 h induced in crease of Cav3.1 but not Cav3.2 mRNA expression in HL-1 cells and the increase was inhibited by BMP4 inhibitor noggin.Acute treatment with BMP4 did not affect T-type Ca2 + currents, but chronic treatment (48 h) significantly increased the ampli tude of T-type Ca2+ currents in HL-1 cells.Chronic treatment with BMP4 induced up-regulation of NADPH oxidase-4 (NOX4), increase of ROS level and activation of MAPK-activated protein kinases JNK and p38.BMP4-induced up-regulation of Cav3.1 mRNA was inhibited by NADPH oxidase inhibitor apocynin, the radical scavenger tempol, JNK in hibitor SP600125 and p38 inhibitor SB203580.In conclusion, BMP4 induces up-regulation of Cav3.1 Ca2+ channels and T-type Ca2+ currents in HL-1 a trial myocytes through ROS/MAPKs pathways.