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Cardiovascular Research 2000 47(1):116-123; doi:10.1016/S0008-6363(00)00061-4
© 2000 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Calcium handling and cell contraction in rat cardiomyocytes depleted of intracellular magnesium

Elinor J Griffiths*

Bristol Heart Institute, University of Bristol, Bristol, UK

* Tel.: +44-117-928-3586; fax: +44-117-928-3581 elinor.griffiths{at}bristol.ac.uk

Objectives: Depressed levels of cardiac Mg have been found in patients with ischaemic heart disease or heart failure, but it is not known whether low intracellular free [Mg2+] ([Mg2+]i) is a causal factor in such myocardial dysfunction. The aims for the present study were to develop a method of lowering [Mg2+]i in myocytes isolated from normal rat hearts, and so to determine whether a low [Mg2+]i itself would cause abnormalities of intracellular Ca2+ ([Ca2+]i) homeostasis or myocyte contractile function in absence of any cardiac disease. Methods: Rat ventricular myocytes were loaded with mag-indo-1/AM or indo-1/AM for determination of total [Mg2+]i and [Ca2+]i, respectively. Mitochondrial [Ca2+] was determined by selective loading of indo-1/AM into the mitochondria. Cell contraction was measured using an edge-tracking device. Myocytes were depleted of [Mg2+]i by incubation in absence of external Mg2+. This resulted in a decrease in [Mg2+]i from about 1.3 to 0.3 mM. In subsequent experiments, 1.2 mM MgCl2 was again present in the superfusate. Results: Under basal conditions (low rate of stimulation, 0.2 Hz, and 1 mM external [Ca2+]), the Mg-depleted cells showed very similar changes in [Ca2+] to control cells, despite an increase in the amplitude of cell contraction. But in presence of high external [Ca2+] (4 mM) and 5 Hz stimulation rate, the Mg-depleted cells showed defects in systolic Ca2+ handling and in cell contraction; in particular, they were unable to increase systolic [Ca2+] in response to the stimulus, unlike control cells. Despite these alterations in total [Ca2+]i, mitochondrial Ca2+ uptake was unchanged in the Mg-depleted cells. Conclusions: A low [Mg2+]i can itself cause significant cardiomyocyte dysfunction in absence of any contributing disease state.

KEYWORDS Calcium (cellular); Ion transport; Mitochondria; Myocytes


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