Sodium influx via a non-selective pathway activated by the removal of extracellular divalent cations: possible role in the calcium paradox

Bosteels, Suzanne

doi:10.1016/s0008-6363(99)00098-x

Cited by 20 publications

(31 citation statements)

References 28 publications

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“…Allen's group also showed that GsMTx4 inhibits the Ca 2+ elevation of stretched mdx muscle fibers (Yeung et al, 2005). As well as the muscle MSCs being permeant to Ca 2+ , Na + influx can indirectly lead to Ca 2+ elevation through the Na + /Ca 2+ exchanger (Arnon et al, 2000;Bosteels et al, 1999). .…”

Section: Potential Therapeutic Targets For Gsmtx4 Cardiac Arrhythmiasmentioning

confidence: 99%

Mechanosensitive ion channels and the peptide inhibitor GsMTx-4: History, properties, mechanisms and pharmacology

Bowman

Gottlieb

Suchyna

et al. 2007

Toxicon

160

120

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Section: Potential Therapeutic Targets For Gsmtx4 Cardiac Arrhythmiasmentioning

confidence: 99%

Mechanosensitive ion channels and the peptide inhibitor GsMTx-4: History, properties, mechanisms and pharmacology

Bowman

Gottlieb

Suchyna

et al. 2007

Toxicon

160

120

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“…The main findings include the following: (1) a rise in basal metabolism that relates not only to the already reported increase in Na + i (Bhojani & Chapman 1990, Jansen et al. 1998, Bosteels et al. 1999) but also to an increased Ca 2+ i ; (2) the changes in heat rate fraction associated with Ca 2+ ‐dependent transport processes were quantitatively the most important ones; (3) both mit‐CaU and mit‐NCE are involved in the myothermic response to extracellular Ca 2+ withdrawal; and (4) the altered cellular ionic homeostasis would trigger a mitochondrial Ca 2+ cycling that contributes to the energetically more expensive basal metabolism maintenance under 0Ca 2+ .…”

Section: Discussionmentioning

confidence: 85%

“…It is known that Ca 2+ ‐free perfusion elicits Na + influx into cardiomyocytes (Bhojani & Chapman 1990, Jansen et al. 1998, Bosteels et al. 1999).…”

Section: Discussionmentioning

confidence: 99%

Cardiac basal metabolism: energetic cost of calcium withdrawal in the adult rat heart

Bonazzola

Takara

2010

Acta Physiologica

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Energy expenditure for resting state maintenance upon calcium withdrawal depends on the intracellular rise in both sodium and calcium. Our data are consistent with a mitochondrial Ca(2+) cycling, not detectable under normal calcium diastolic levels. The experimental condition here analysed, partially simulates findings reported under certain pathological situations including heart failure in which mildly increased levels of both diastolic sodium and calcium have also been found. Therefore, under such pathological conditions, hearts should distract chemical energy to fuel processes associated with sodium and calcium handling, making more expensive the maintenance of their functions.

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“…Because each well of the 96-well plate that we used in our experiment was also a closed space, the gradual increase of fluorescence intensity after recording for a 60-minute period, at which time the completion of hydrolysis was expected [6], was speculated to be the result of dye leakage. Probenecid, an organic anion transport blocker, has been reported to prevent Fura-2 leakage from cells, and this effect has also been reported for SBFI used to measure [Na + ] i [16]. Cao, et al reported the value of [Na + ] i in neocortical neurons, and demonstrated that several compounds induced changes in [Na + ] i using a microplate reader with a 96-well format [17].…”

Section: Resultsmentioning

confidence: 95%

A technique for quantifying intracellular free sodium ion using a microplate reader in combination with sodium-binding benzofuran isophthalate and probenecid in cultured neonatal rat cardiomyocytes

et al. 2013

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BackgroundIntracellular sodium ([Na+]i) kinetics are involved in cardiac diseases including ischemia, heart failure, and hypertrophy. Because [Na+]i plays a crucial role in modulating the electrical and contractile activity in the heart, quantifying [Na+]i is of great interest. Using fluorescent microscopy with sodium-binding benzofuran isophthalate (SBFI) is the most commonly used method for measuring [Na+]i. However, one limitation associated with this technique is that the test cannot simultaneously evaluate the effects of several types or various concentrations of compounds on [Na+]i. Moreover, there are few reports on the long-term effects of compounds on [Na+]i in cultured cells, although rapid changes in [Na+]i during a period of seconds or several minutes have been widely discussed.FindingsWe established a novel technique for quantifying [Na+]i in cultured neonatal rat cardiomyocytes attached to a 96-well plate using a microplate reader in combination with SBFI and probenecid. We showed that probenecid is indispensable for the accurate measurement because it prevents dye leakage from the cells. We further confirmed the reliability of this system by quantifying the effects of ouabain, which is known to transiently alter [Na+]i. To illustrate the utility of the new method, we also examined the chronic effects of aldosterone on [Na+]i in cultured cardiomyocytes.ConclusionsOur technique can rapidly measure [Na+]i with accuracy and sensitivity comparable to the traditional microscopy based method. The results demonstrated that this 96-well plate based measurement has merits, especially for screening test of compounds regulating [Na+]i, and is useful to elucidate the mechanisms and consequences of altered [Na+]i handling in cardiomyocytes.

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Sodium influx via a non-selective pathway activated by the removal of extracellular divalent cations: possible role in the calcium paradox

Abstract: A cation non-selective conductance, different from L-type Ca2+ channels, contributes to the Nai+ accumulation obtained during perfusion with Ca2+/Mg(2+)-free media, hence also to the Cai2+ overload and cellular damage upon Cao2+ repletion (the Ca2+ paradox).

Cited by 20 publications

References 28 publications

Mechanosensitive ion channels and the peptide inhibitor GsMTx-4: History, properties, mechanisms and pharmacology

Mechanosensitive ion channels and the peptide inhibitor GsMTx-4: History, properties, mechanisms and pharmacology

Cardiac basal metabolism: energetic cost of calcium withdrawal in the adult rat heart

A technique for quantifying intracellular free sodium ion using a microplate reader in combination with sodium-binding benzofuran isophthalate and probenecid in cultured neonatal rat cardiomyocytes

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