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Mechanisms for monovalent cation‐dependent depletion of intracellular Mg2+:Na+‐independent Mg2+ pathways in guinea‐pig smooth muscle

It has been suggested that magnesium deficiency is correlated with many diseases. 31P NMR experiments were carried out in order to investigate the effects of Na+ substitution on Mg2+ depletion in smooth muscle under divalent cation‐free conditions. In the taenia of guinea‐pig caeci, the intracellular free Mg2+ concentration ([Mg2+]i) was estimated from the chemical shifts of (1) the β‐ATP peak alone and (2) β‐ and γ‐ATP peaks. Both estimations indicated that [Mg2+]i decreased only very slowly in Mg2+‐free, Ca2+‐free solutions in which Na+ was substituted with large cations such as NMDG (N‐methyl‐D‐glucamine) and choline. Furthermore, the measurements of tension development supported the suggestion of preservation of intracellular Mg2+ with NMDG substitution. Substituting extracellular Na+ with the small cation, Li+, also shifted the β‐ATP peak towards a lower frequency, but the frequency shift was significantly less than that seen upon Na+ substitution with K+. The estimated [Mg2+]i depletion was, however, comparable with that seen after Na+ substitution with K+ using the titration curves of metal‐free and Mg2+‐bound ATP obtained in Li+‐based model solutions. It was concluded that Mg2+ rapidly decreases only when small cations were the major electrolyte of the extracellular medium. Na+ substitutions with NMDG, choline or Li+ had little effect on intracellular ATP concentration after 100 min treatment.