Mg inhibits voltage and tension oscillation but potentiates twitch in depolarized myocardium.

In the presence of 1-5 X 10(-8) M isoproterenol, guinea pig ventricular muscle, depolarized by K-rich (27 mM) solution, exhibits a biphasic twitch tension, after contraction (AC), and oscillatory afterpotentials (OAP) in response to 1-Hz stimulation. We obtained data suggesting that OAP and AC are due to a spontaneous oscillatory release of Ca from the sarcoplasmic reticulum (SR) and that the initial component (C1) of the biphasic twitch, which produces a large and early peak in tension, reflects the excitation-coupled Ca release from SR. Elevation of extracellular Mg concentration ([Mg]o) to 3-6 mM suppressed AC and OAP. However, C1 was markedly potentiated by high [Mg]o. When single extrasystoles with various coupling intervals were interposed during a regular stimulation at 0.2 Hz, C1 in the extrasystole, which was large with a short coupling interval, gradually decreased with lengthening of the coupling interval. Elevation of [Mg]o markedly reduced the rate of this decrease suggesting that the decrease in available Ca in the SR during diastole was slowed by high [Mg]o. Thus, in depolarized ventricle, high Mg solution seems to depress the spontaneous oscillatory Ca release from SR and subsequently enhances the Ca release coupled to membrane excitation. The latter enhancement may be related to stabilization of the Ca in SR during diastole.