Key result
Sodium ion, and to a lesser extent lithium, reduced calcium accumulation by cardiac sarcoplasmic reticulum through rapid release of bound radiocalcium.
Sodium ions reduce calcium binding in cardiac sarcoplasmic reticulum by inducing rapid release of bound calcium, potentially playing a role in tension regulation.
Offers mechanistic clues for cardiac tension regulation; leaves open translation to human physiology.
The effects of monovalent cations on the active calcium-accumulating ability of cardiac sarcoplasmic reticulum were assessed. Grana prepared in an ion-free system accumulated calcium when ATP and Mg(++) were present. Sodium ion and to a lesser extent lithium but not K(+) reduced the amount of calcium taken up. The reduction of calcium binding by Na(+) is not due to inhibition of uptake but to a rapid release of the radiocalcium bound. The amount of calcium released by sodium does not appear to be enough to explain contraction on the basis of sodium influx into muscle, but may be significant in the regulation of tension.
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Palmer et al. (1967) studied this question. Monovalent cations (Sodium, Lithium, Potassium) vs. Ion-free system was evaluated on Active calcium-accumulating ability. Sodium ion, and to a lesser extent lithium, reduced calcium accumulation by cardiac sarcoplasmic reticulum through rapid release of bound radiocalcium.
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