Comparison of the effects of internal [Mg2+] on IK1 in cat and guinea-pig cardiac ventricular myocytes

The effects of internal Mg 2+ (Mg 2+ i on processes underlying the inward rectification of the cardiac I Kl in enzymatically isolated cardiac ventricular myocytes (CVM) obtained from cat, guinea pig and rabbit were compared using the whole-cell and excised inside-out patch configurations of the voltage-clamp technique. In confirmation of the findings of other investigators, Mg 2+ i -sensitive outward I Kl currents could be elicited from guinea pig CVM at 15°C when Mg 2+ i was reduced from 1 m M to less than 1 α M , suggesting that Mg 2+ i has an important role in the inward rectification of I Kl in guinea pig CVM at unphysiologically low temperatures. However, as temperature was raised to more physiological levels, (e.g., 30°C), Mg 2+ i -sensitive outward I Kl currents could no longer be evoked. In contrast with the results obtained with guinea pig CVM I Kl remained inwardly rectifying in cat and rabbit CVM independent of the Mg 2+ i concentration ([Mg 2+ ] i ) at 37°, 15°, 10° and 5°C. Reduced [Mg 2+ ] i at low temperature (15°C), shifted the voltage dependence of guinea pig I Kl activation in the depolarizing direction; this resulted in an apparent linearization of I KI conductance. When the range of the membrance potential examined was expanded to include voltages up to +80 mV, the guinea pig I Kl was found to exhibit inward rectification with the inflection in the I-V relationship that is found at ~E K at normal temperature, also shifted 80 mV or more to much less negative voltages at low temperatures. In contrast, irrespective of [Mg 2+ ] l or temperature, the voltage dependencies of the I Kl activation curves for both cat and rabbit myocytes were not changed from that defined when [Mg 2+ ] i was m M and temperature was 37°C. We propose that Mg 2+ i affects inward rectification of I KI on cold guinea pig CVM by altering the voltage dependence of activation.