Gd³⁺ blocks stretch-activated channels and suppresses stretch-induced arrhythmias. We used whole cell voltage clamp to examine whether effects on Na⁺ channels might contribute to the antiarrhythmic efficacy of Gd³⁺. Gd³⁺ inhibited Na⁺ current (I_Na) in rabbit ventricle (IC₅₀ = 48 µM at 35 mV, holding potential 120 mV), and block increased at more negative test potentials. Gd³⁺ made the threshold for I_Na more positive and reduced the maximum conductance. Gd³⁺ (50 µM) shifted the midpoints for activation and inactivation of I_Na 7.9 and 5.7 mV positive but did not alter the slope factor for either relationship. Activation and inactivation kinetics were slowed in a manner that could not be explained solely by altered surface potential. Paradoxically, Gd³⁺ increased I_Na under certain conditions. With membrane potential held at 75 mV, Gd³⁺ still shifted threshold for activation positive, but I_Na increased positive to 40 mV, causing the current-voltage curves to cross over. When availability initially was low, increased availability induced by Gd³⁺ dominated the response at test potentials positive to 40 mV. The results indicate that Gd³⁺ has complex effects on cardiac Na⁺ channels. Independent of holding potential, Gd³⁺ is a potent I_Na blocker near threshold potential, and inhibition of I_Na by Gd³⁺ is likely to contribute to suppression of stretch-induced arrhythmias.