Transforming growth factors- (TGF-s) are essential to the structural remodeling seen in cardiac disease and development; however, little is known about potential electrophysiological effects. We hypothesized that chronic exposure (6-48 h) of primary cultured neonatal rat cardiomyocytes to the type 1 TGF- (TGF-1; 5 ng ml^-1), may affect voltage-dependent Ca²⁺ channels. Thus, we investigated T- (I_CaT) and L-type (I_CaL) Ca²⁺ currents, as well as dihydropyridine-sensitive charge movement using the whole-cell patch-clamp technique, and quantified Ca_V1.2 mRNA levels by real-time PCR assay. In ventricular myocytes, TGF-1 did not exert significant electrophysiological effects. However, in atrial myocytes, TGF-1 reduced both I_CaL and charge movement (55% at 24-48 h), without significantly altering I_CaT, cell membrane capacitance, or channel kinetics (voltage-dependence of activation and inactivation, as well as the activation and inactivation rates). Reductions of I_CaL and charge movement were explained by concomitant effects on the maximal values of L-channels conductance (G_max) and charge movement (Q_max). Thus, TGF-1 selectively reduces the number of functional L-channels on the surface of plasma membrane, in atrial but not ventricular myocytes. The TGF-1-induced I_CaL reduction was unaffected by supplementing intracellular recording solutions with okadaic acid (2 µM) or cAMP (100 µM), two compounds that promote L-channel phosphorylation. This suggests that I_CaL reduction cannot be explained by a possible regulation in the L-channels phosphorylation state. Instead, we found that TGF-1 decreases the expression levels of atrial Ca_V1.2 mRNA (70%). Thus, TGF-1 downregulates atrial L-channel expression, and may be therefore contributing to the in-vivo cardiac electrical remodeling.