Abstract
1. Neutral carrier-based liquid membrane micro-electrodes were constructed which are suitable for continuous measurements of [Mg2+]i in cardiac and skeletal muscle preparations.
2. The electrodes show a Nernstian behaviour in pure MgCl2 solutions. In the presence of a constant ionic background chosen to simulate the cytoplasmic composition, the calibration function flattens progressively with lower [Mg2+], due to the interference of K+ and Na+. The response to changes in [Mg2+] is less than 0·5 sec.
3. In quiescent preparations at room temperature (23 °C), the following basal [Mg2+]i were determined: 3·5 mM (sheep Purkinje fibres), 3·1 mM (sheep ventricular muscle), 3·0 mM (ferret ventricular muscle) and 3·3 mM (frog skeletal muscle).
4. In cardiac tissue, electrical stimulation does not measurably affect the basal [Mg2+]i.
5. In the presence of 0·5 mM-Mg2+o, the calculated Mg2+ equilibrium potentials, EMg, are in the range of -23 to -25 mV, suggesting that Mg2+ is not passively distributed across the sarcolemma in striated muscle.
6. Further studies were performed on sheep Purkinje fibres to investigate the effect of various experimental interventions on [Mg2+]i.
7. Elevating [Mg2+]o from 0·5 to 10 mM resulted in a reversible increase of [Mg2+]i. The initial rate of increase corresponds to a Mg2+ influx of 0·42 p-mole/cm2.sec, or a magnesium permeability, PMg, of 1·6 × 10-8cm/sec.
8. Increasing PCO2 from nominally 0 to 100 mmHg (Tris-buffered vs. bicarbonate-buffered Tyrode solution) produced a reversible decrease in [Mg2+]i by roughly 0·45 mM, probably due to Mg2+ binding the newly formed intracellular HCO3-.
9. The effect of metabolic poisoning on [Mg2+]i was assessed by exposure to cyanide, iodoacetic acid and 2-4-dinitrophenol. No significant increase in [Mg2+]i indicative of a liberation of Mg2+ from ATP was observed.
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