Clinical studies have shown that the rate of VA in hypertensive patients with LVH was several times higher than the normaltensive ones. Currently the mechanism of VA due to LVH is not yet fully clarified. Growing evidences indicate that microRNAs (miRNAs or miRs) are regulators of gene expression, which are becoming increasingly recognised as important regulators of heart function and diseases. Here we observed that miR-1 was striking because of its more than (2.08±0.21) fold increased in the spontaneously hypertensive rat model (SHRs) with LVH. miR-1 overexpression slowed conduction and depolarised the cytoplasmic membrane by post-transcriptionally repressing Kir2.1 and connexin 43(Cx43), and this likely accounts at least in part for its arrhythmogenic potential. Then we confirmed that in vivo suppression of miR-1 in SHRs could upgrade Cx43 and Kir2.1 protein level. Our data show that miR-1 is a key regulator of cardiac hypertrophy formation and VA due to LVH, suggesting its attractive therapeutic application in ventricular arrhythmia occurred in the hypertensive heart.