Cardiac hypertrophy is associated with electrical modifications, including sustained depolarisation and modification of action potential, that lead to a propensity for arrhythmias. Ionic currents such as I_f, I_Ca-T and I_to participate in these modifications. In addition, we previously reported the appearance of a Ca²⁺-activated non-selective cation current (NSC_Ca) in adult cardiomyocyte culture, which has been proposed as an in vitro model of cardiac hypertrophy (Guinamard et al. 2002). In the same way, we report in the present study, an enhanced expression of this current on freshly isolated cells from spontaneously hypertensive rats (SHR) known to develop cardiac hypertrophy. Cells were isolated from the left ventricles of hearts from 3 to 6 month old Wistar Kyoto or SHR male rats using both enzymatic and mechanical dissociation processes. Animals were humanely killed in accordance with the European Community Council Directive. Before patching, cells were incubated for at least 10 min with 500 nM phorbol 12-myristate, 13-acetate (PMA), a PKC activator that activates the cardiac NSCCa (Guinamard et al. 2004). Channel activity was recorded in inside-out patches with a solution (bath and pipette) containing (mM): 140 NaCl, 4.8 KCl, 1.2 MgCl₂, 1 CaCl₂, 10 glucose and 10 Hepes. In these ionic conditions, the channel exhibited a linear current-voltage relationship (γ = 23.3 ± 1.1 pS, n = 4). Channel activity increased with depolarisation. Open probability as a function of voltage was fitted to a Boltzmann function with values of 15.5 for s and +43.8 mV for V_0.5. The channel discriminated poorly among monovalent cations (Na⁺, K⁺) and was impermeable to Cl^– (P_Cl/P_Na = 0.08). Reducing internal calcium to 10^-9 M abolished channel activity. These properties are similar to those previously reported on dedifferentiated rat ventricular myocytes (Guinamard et al. 2002). NSC_Ca channel activity, which was rarely detected in cardiac cells from normotensive rats (7.3% of patches, n = 41) even after PMA treatment was frequently recorded in myocytes from SHR rats (43.8% of patches, n = 16). Cardiac hypertrophy was associated with a prolongation of the QT interval on the ECG. The increase in NSC_Ca channel occurrence observed during cardiac hypertrophy, which increased the Na⁺ influx, would participate in slowing repolarisation. In addition, activation of the channel will be able to modify the resting membrane potential to a less negative value leading to more excitable cells. Thus the NSC_Ca may play a primary role in the genesis of arrhythmias. The NSC_Ca channel shares the hallmarks of the TRPM4 channel (Launay et al. 2002).