Magnesium homeostasis in cardiac myocytes of Mg-deficient rats
To study possible modulation of Mg(2+) transport in low Mg(2+) 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...
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Published in | PloS one Vol. 8; no. 9; p. e73171 |
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Abstract | To study possible modulation of Mg(2+) transport in low Mg(2+) 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 Mg(2+) concentration ([Mg(2+)]i) of ventricular myocytes was measured with the fluorescent indicator furaptra. Mg(2+) transport rates, rates of Mg(2+) influx and Mg(2+) efflux, were estimated from the rates of change in [Mg(2+)]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 [Mg(2+)]i of ventricular myocytes was significantly different between Mg-deficient rats and control rats. The rates of Mg(2+) 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 Mg(2+) channels/transporters (TRPM6, TRPM7, MagT1, SLC41A1 and ACDP2) in heart and kidney tissues. These results suggest that [Mg(2+)]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 Mg(2+) channels/transporters in the heart. |
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AbstractList | 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. To study possible modulation of Mg 2+ transport in low Mg 2+ 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 Mg 2+ concentration ([Mg 2+ ] i ) of ventricular myocytes was measured with the fluorescent indicator furaptra. Mg 2+ transport rates, rates of Mg 2+ influx and Mg 2+ efflux, were estimated from the rates of change in [Mg 2+ ] 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 [Mg 2+ ] i of ventricular myocytes was significantly different between Mg-deficient rats and control rats. The rates of Mg 2+ 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 Mg 2+ channels/transporters (TRPM6, TRPM7, MagT1, SLC41A1 and ACDP2) in heart and kidney tissues. These results suggest that [Mg 2+ ] 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 Mg 2+ channels/transporters in the heart. To study possible modulation of Mg(2+) transport in low Mg(2+) 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 Mg(2+) concentration ([Mg(2+)]i) of ventricular myocytes was measured with the fluorescent indicator furaptra. Mg(2+) transport rates, rates of Mg(2+) influx and Mg(2+) efflux, were estimated from the rates of change in [Mg(2+)]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 [Mg(2+)]i of ventricular myocytes was significantly different between Mg-deficient rats and control rats. The rates of Mg(2+) 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 Mg(2+) channels/transporters (TRPM6, TRPM7, MagT1, SLC41A1 and ACDP2) in heart and kidney tissues. These results suggest that [Mg(2+)]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 Mg(2+) channels/transporters in the heart. To study possible modulation of Mg.sup.2+ transport in low Mg.sup.2+ 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 Mg.sup.2+ concentration ([Mg.sup.2+ ].sub.i) of ventricular myocytes was measured with the fluorescent indicator furaptra. Mg.sup.2+ transport rates, rates of Mg.sup.2+ influx and Mg.sup.2+ efflux, were estimated from the rates of change in [Mg.sup.2+ ].sub.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 [Mg.sup.2+ ].sub.i of ventricular myocytes was significantly different between Mg-deficient rats and control rats. The rates of Mg.sup.2+ 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 Mg.sup.2+ channels/transporters (TRPM6, TRPM7, MagT1, SLC41A1 and ACDP2) in heart and kidney tissues. These results suggest that [Mg.sup.2+ ].sub.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 Mg.sup.2+ channels/transporters in the heart. |
Audience | Academic |
Author | Inoue, Hana Tashiro, Michiko Konishi, Masato |
AuthorAffiliation | The University of Manchester, United Kingdom Department of Physiology, Tokyo Medical University, Tokyo, Japan |
AuthorAffiliation_xml | – name: Department of Physiology, Tokyo Medical University, Tokyo, Japan – name: The University of Manchester, United Kingdom |
Author_xml | – sequence: 1 givenname: Michiko surname: Tashiro fullname: Tashiro, Michiko organization: Department of Physiology, Tokyo Medical University, Tokyo, Japan – sequence: 2 givenname: Hana surname: Inoue fullname: Inoue, Hana – sequence: 3 givenname: Masato surname: Konishi fullname: Konishi, Masato |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24039880$$D View this record in MEDLINE/PubMed |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Conceived and designed the experiments: MT HI MK. Performed the experiments: MT HI. Analyzed the data: MT HI. Wrote the paper: MT MK. Competing Interests: The authors have declared that no competing interests exist. |
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Snippet | To study possible modulation of Mg(2+) transport in low Mg(2+) conditions, we fed either a Mg-deficient diet or a Mg-containing diet (control) to Wistar rats... To study possible modulation of Mg.sup.2+ transport in low Mg.sup.2+ conditions, we fed either a Mg-deficient diet or a Mg-containing diet (control) to Wistar... 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... To study possible modulation of Mg 2+ transport in low Mg 2+ conditions, we fed either a Mg-deficient diet or a Mg-containing diet (control) to Wistar rats for... |
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SubjectTerms | Absorption spectroscopy Animal tissues Animals Atomic absorption analysis Atomic absorption spectroscopy Atomic beam spectroscopy Biological Transport Body Weight Cardiac muscle Cardiomyocytes Cation Transport Proteins - genetics Cation Transport Proteins - metabolism Cell Membrane - metabolism Channels Diet Efflux Extracellular Space - metabolism Fluorescence Gene Expression Genomics Heart Heart diseases Heart Ventricles - metabolism Homeostasis Hypomagnesemia Kidneys Magnesium Magnesium - blood Magnesium - metabolism Magnesium Deficiency - genetics Magnesium Deficiency - metabolism Male Minerals - blood Minerals - metabolism Modulation Myocytes Myocytes, Cardiac - metabolism Physiology Polymerase chain reaction Proteins Rats RNA Rodents Spectral analysis Spectroscopy Spectrum analysis Transient receptor potential proteins Transport Ventricle |
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Title | Magnesium homeostasis in cardiac myocytes of Mg-deficient rats |
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