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The Ca2+ sensitivity of a population of isolated adult rat heart myocytes has been related to the Na+ content of the cells prior to Ca2+ exposure, and the intracellular free Ca2+ as reported by quin2 fluorescence when the cells are challenged with millimolar external Ca2+. Myocytes exposed to Ca2+ during quin2 loading show a resting intracellular free Ca2+ of 150 +/- 30 nM and retain the rod cell morphology of heart cells in situ. The myocytes take up Na+ and lose K+ when incubated in the cold in the absence of Ca2+. Large numbers of these rod-shaped, Na+-loaded myocytes hypercontract into grossly distorted round cell forms when exposed to physiological levels of Ca2+. The number of cells that hypercontract is proportional to the Na+ content of the cells prior to Ca2+ addition and can be directly related to the intracellular free Ca2+ concentration attained following Ca2+ addition. Fifty percent of the cells in a myocyte population hypercontract when the internal free Ca2+ concentration reported by quin2 reaches 400 nM and virtually all of the cells hypercontract when this value reaches 1 microM. The entry of Ca2+ into Na+-loaded myocytes is biphasic with one phase inhibited by Ca2+ channel blockade. This suggests that Ca2+ enters Na+-loaded myocytes by the Ca2+ channel as well as by Na+/Ca2+ exchange.
M R Lambert, and
J D Johnson, and
K G Lamka, and
G P Brierley, and
R A Altschuld
May 1984,
Canadian journal of physiology and pharmacology,
M R Lambert, and
J D Johnson, and
K G Lamka, and
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September 1997,
Cellular and molecular biology (Noisy-le-Grand, France),
M R Lambert, and
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June 1988,
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M R Lambert, and
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Biochimica et biophysica acta,
M R Lambert, and
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February 1993,
Clinical science (London, England : 1979),
M R Lambert, and
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August 1985,
Biochimica et biophysica acta,
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Japanese heart journal,
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M R Lambert, and
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September 2013,
Anesthesiology,
