Abstract
To study possible modulation of Mg2+ transport in low Mg2+ conditions, we fed either a Mg-deficient diet or a Mg-containing diet (control) to Wistar rats for 1–6 weeks. Total Mg concentrations in serum and cardiac ventricular tissues were measured by atomic absorption spectroscopy. Intracellular free Mg2+ concentration ([Mg2+]i) of ventricular myocytes was measured with the fluorescent indicator furaptra. Mg2+ transport rates, rates of Mg2+ influx and Mg2+ efflux, were estimated from the rates of change in [Mg2+]i during Mg loading/depletion and recovery procedures. In Mg-deficient rats, the serum total Mg concentration (0.29±0.026 mM) was significantly lower than in control rats (0.86±0.072 mM) after 4–6 weeks of Mg deficiency. However, neither total Mg concentration in ventricular tissues nor [Mg2+]i of ventricular myocytes was significantly different between Mg-deficient rats and control rats. The rates of Mg2+ influx and efflux were not significantly different in both groups. In addition, quantitative RT-PCR revealed that Mg deficiency did not substantially change mRNA expression levels of known Mg2+ channels/transporters (TRPM6, TRPM7, MagT1, SLC41A1 and ACDP2) in heart and kidney tissues. These results suggest that [Mg2+]i as well as the total Mg content of cardiac myocytes, was well maintained even under chronic hypomagnesemia without persistent modulation in function and expression of major Mg2+ channels/transporters in the heart.
Highlights
Intracellular Mg2+ plays crucial roles in cellular functions, including DNA synthesis, enzyme activities, and gating of ion channels
The serum Mg concentration quickly decreased after starting the Mg-deficient diet, and was significantly lower than the control rats after 2 weeks of feeding (Fig. 2B)
In the rats fed the control diet the serum Mg concentration remained approximately constant at 0.9–1 mM throughout the feeding period (1–6 weeks) (Fig. 2B)
Summary
Intracellular Mg2+ plays crucial roles in cellular functions, including DNA synthesis, enzyme activities, and gating of ion channels. Regarding the physiological condition of rat ventricular myocytes, the intracellular free Mg2+ concentration ([Mg2+]i) is in the range of 0.8–1.0 mM [6], and it is thought to be regulated by the balance between passive influx driven by the electrochemical gradient of ion and active extrusion in exchange for Na+ influx (i.e., putative Na+/Mg2+ exchange). The melastatin subfamily 6 and 7 of the transient receptor potential cation channels (TRPM6 and 7, respectively) [8,9,10,11], MagT1 [12], SLC41A1 [13] and ACDP2 [14] are suggested to be the Mg2+ channels/transporters implicated in Mg2+ homeostasis of mammalian cells. It has been reported that the function and expression of such Mg2+ channels/transporters are modified by extracellular and intracellular levels of Mg2+.
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