Whole cell voltage-clamp techniques were used to study the effects of extracellular Mg2+ on T- and L-type Ca2+ currents recorded from single atrial myocytes from cat heart. T and L currents were distinguished primarily by their voltage dependence. With 5.4 mM Ca2+ as charge carrier, maximal T- and L-current densities were 1.0 +/- 0.06 and 9.7 +/- 0.4 pA/pF, respectively. Nickel (Ni2+, 50-mu-M) inhibited maximal T current (-65.6 +/- 5.9%) more than L current (-15.7 +/- 2.4%), and 10-mu-M cadmium (Cd2+) inhibited L current (-65.5 +/- 5.9%) without significant effect on T current (-8.7 +/- 8.1%). Mg2+ elicited a dose-dependent inhibition of both T and L currents. Mg2+ < 8.4 mM inhibited T current more than L current. At Mg2+ greater-than-or-equal-to 8.4 mM, T-current inhibition reach a plateau at approximately 52%, whereas L current was further inhibited (-65%) at 16.8 mM Mg2+. Mg2+ elicited a dose-dependent positive shift in half-maximal voltages of activation and inactivation for both T and L currents. Mg2+ -induced inhibition of both T and L currents was greater in lower (2.7 mM) external Ca2+. Finally, 4.2 mM mg2+ and 50-mu-M Ni2+ elicited a similar decrease in the late diastolic slope of subsidiary pacemaker action potentials, whereas 10-mu-M Cd2+ markedly inhibited action potential amplitude. In conclusion, elevated Mg2+ inhibits both T- and L-type Ca2+ currents, although the sensitivity and maximal response of each current differs. Mg2+ is less effective and less specific than Ni2+ or Cd2+ in inhibiting T and L currents, respectively. T current may participate in the late diastolic slope of subsidiary pacemakers. Inhibition of T-type Ca2+ currents may contribute to the antiarrhythmic effects of Mg2+ in atrial muscle.