INTRACELLULAR MG2-PIG VENTRICULAR MYOCYTES( DEPLETION DEPRESSES THE DELAYED RECTIFIER K+ CURRENT IN GUINEA)

The effects of various [Mg2+](i), particularly low [Mg2+](i), on the d elayed rectifier K+ current (I-K) were studied in guinea pig ventricul ar myocytes with the patch, clamp technique. The magnitude of I-K was evaluated from the amplitude of its tail current elicited on repolariz ation following the depolarizing steps. The pipette-perfusion techniqu e was also used. The initial variations of I-K magnitude were dependen t on [Mg2+](i) in the internal solutions with which the whole-cell rec ording was begun. With 0.03 to 1 mM [Mg2+](i), I-K was relatively stab le after patch rupture, showing a minimal decay with time; with 3 mM [ Mg2+](i), I-K rapidly declined; with [Mg2+](i), less than 0.01 mM I-K transiently increased after patch break, but declined progressively th ereafter as the magnitude of I-K decreased to about 30% of the initial magnitude in 10 min. The decline of I-K at low [Mg2+](i) showed the f ollowing features. The decline was accompanied little by changes in th e voltage-activation relation or by changes in the kinetics of current deactivation. The decline was not related to changes in [Ca2+](i) and was also observed in ATP gamma S-loaded, isoprenaline-stimulated cell s, in which I-K channels were presumed to be persistently phosphorylat ed. An application of okadaic acid did not prevent the decline of I-K during Mg2+ depletion. It is suggested that a presence of [Mg2+](i) hi gher than 0.01 mM is required to maintain I-K in guinea pig ventricula r cells. The depression of I-K at low [Mg2+](i) appears to involve a p hosphorylation-dephosphorylation-independent mechanism.