Recently, it has been revealed that angiotensin II type 1 receptor (AT 1 ) antagonists act as antiarrhythmic agents and that the T-type Ca 2+ channel plays an important role in arrhythmia. However, it remains unclear how the T-type Ca 2+ channel expression system is involved in angiotensin II-mediated arrhythmogenesis in cardiomyocytes. In this study, we investigated the effect of telmisartan, an AT 1 receptor antagonist, on transcriptional regulation of T-type Ca 2+ channel isoform (Ca v 3.1 and Ca v 3.2) expression and cardiac contractility using rat neonatal cardiomyocytes. Cultured cardiomyocytes were stimulated with telmisartan and/or angiotensin II for 24 h. T-type Ca 2+ currents (I Ca.T ) were then measured with the patch clamp technique, while Ca v 3.1 and Ca v 3.2 mRNA expression were assessed by real-time PCR. Expression of Ca v 3.1 and Ca v 3.2 mRNA as well as I Ca.T current density in cardiomyocytes increased significantly after long-term application of angiotensin II (24 h), which was accompanied by extracellular signal-regulated kinase (ERK)1/2 and p38 mitogen-activated protein kinase (MAPK) phosphorylation. In contrast, telmisartan decreased Ca v 3.1 and Ca v 3.2 mRNA expression as well as I Ca.T in a dose-dependent manner in the absence of angiotensin II. In addition, the basal phosphorylation level of p38MAPK but not ERK1/2 was decreased by telmisartan in the absence of angiotensin II. Valsartan, an AT 1 receptor antagonist, did not mimic the action of telmisartan, while the action of telmisartan was completely blocked by valsartan. These results indicate that telmisartan attenuates T-type Ca 2+ channel expression likely through p38MAPK activity in an agonist-independent manner, which suggests a novel pharmacological action of telmisartan.