What question did this study set out to answer?

To determine how elevated intracellular magnesium affects the beta-adrenergic stimulation of L-type calcium currents in ventricular myocytes.

December 17, 2012The Journal of General PhysiologyOpen Access

Increased intracellular magnesium attenuates β-adrenergic stimulation of the cardiac CaV1.2 channel

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Why the study?

Does increased intracellular magnesium attenuate beta-adrenergic stimulation of L-type Ca2+ current in adult ventricular myocytes?

Key Points

To determine how elevated intracellular magnesium affects the beta-adrenergic stimulation of L-type calcium currents in ventricular myocytes.
Measured L-type calcium currents in acutely dissociated adult mammalian ventricular myocytes exposed to 0.8 mM versus 2.4 mM intracellular magnesium.
Mapped the site of action by activating signaling intermediates using isoproterenol, forskolin, isobutylmethylxanthine, calyculin A, and (S)-BayK8644.
Elevating intracellular magnesium from 0.8 mM to 2.4 mM attenuated isoproterenol-stimulated L-type calcium current from 75 ± 13% to 20 ± 8%.
Magnesium suppressed channel stimulation by forskolin, IBMX, and calyculin A, but did not alter channel activation by (S)-BayK8644, indicating a direct effect on the CaV1.2 channel.

Structured PICO

Does increased intracellular magnesium attenuate beta-adrenergic stimulation of L-type Ca2+ current in adult ventricular myocytes?

Population

Acutely dissociated adult mammalian ventricular myocytes (VMs)

Intervention

Increased intracellular Mg(2+) concentration (2.4 mM)

Comparator

Lower intracellular Mg(2+) concentration (0.8 mM)

Outcome

Isoproterenol stimulation of the L-type Ca(2+) currentsurrogate

Increased intracellular magnesium directly attenuates beta-adrenergic stimulation of cardiac CaV1.2 channels, which may reduce metabolic stress during transient ischemia.

Discussion

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Implication

May attenuate excessive adrenergic Ca(2+) influx during ischemia in myocytes; hypothesis-generating for magnesium cardioprotection, pending human confirmation.

Cite This Study

Brunet et al. (2012) studied this question.

synapsesocial.com/papers/6a9a86ee141376a341868872 https://doi.org/10.1085/jgp.201210864

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Implication

May attenuate excessive adrenergic Ca(2+) influx during ischemia in myocytes; hypothesis-generating for magnesium cardioprotection, pending human confirmation.

Increased intracellular magnesium attenuates β-adrenergic stimulation of the cardiac CaV1.2 channel

Key Points

Structured PICO

Discussion

Implication

Cite This Study

Increased intracellular magnesium attenuates β-adrenergic stimulation of the cardiac CaV1.2 channel

Key Points

Structured PICO

Discussion

Implication

Cite This Study

Also Consider

Also Consider