Sodium current-induced release of calcium from cardiac sarcoplasmic reticulum

Article Abstract:

The contraction of muscle cells is activated by the release of calcium by internal membranes called the sarcoplasmic reticulum. In skeletal muscle, the release of calcium, and therefore the start of contraction, is directly controlled by changes in voltage of the muscle cell membrane, the scarcolemma. However, this is not the case in heart muscle. In cardiac muscle, the release of calcium by the sarcoplasmic reticulum is thought to be stimulated by calcium arriving through calcium channels in the sarcolemma membrane. Physiological experiments on isolated cardiac muscle cells now suggest that under some conditions, this calcium influx is due to the sodium-calcium exchanger working backwards. Under resting conditions, there is more sodium outside the cell than in, and the energy derived from letting sodium flow in past the exchanger is used to drive calcium ions out. However, a temporary reversal of the sodium concentrates could bring calcium back into the cell, stimulating the sacroplasmic reticulum and the normal events of cell contraction. One of the corollaries of this hypothesis, however, is that the cell is simply too big for the entire internal sodium concentration to change. Therefore, it can only change in a narrow region just inside the cell membrane. Why the sodium ions would not freely diffuse beyond this narrow band is not known. It is worth noting that this hypothetical mechanism would account for the effects of cardiac glycosides such as digitalis, which affect the strength of heart muscle contraction by altering intracellular sodium. (Consumer Summary produced by Reliance Medical Information, Inc.)

Sarcoplasmic reticulum, Sarcolemma

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Atrionatriuretic peptide transforms cardiac sodium channels into calcium-conducting channels

Article Abstract:

Cells of the atria of the heart secrete a substance called atrionatriuretic peptide (ANP) in response to increased extracellular fluid volume. The kidneys respond to this ANP by reducing the resorption of sodium, which results in the production of more urine and a consequent reduction of blood volume. In addition, ANP may regulate its own production by directly affecting the atrial cells themselves. In experiments with rat and guinea pig heart muscle cells, ANP has been shown to change the properties of the sodium channel. Ion channels, in general, are complex protein structures which permit specific ions, such as sodium, potassium, or calcium, to cross the membrane of a cell. In the case of muscle cells, sodium channels are essential for the response of the cell to stimulation, since letting charged ions flow across its membrane is how a cell alters its voltage. Normally, sodium channels are selective for sodium, meaning the resistance of the channel to positively charged ions other than sodium is far greater than the resistance to sodium. However, when measuring the response of the muscle cells in culture dishes, it was found that ANP reduced the permeability of the channel to sodium and increased the permeability of the channel to calcium. In the living heart, this suppression of the sodium current may serve as a feedback mechanism to regulate the secretion of proper amounts of ANP. (Consumer Summary produced by Reliance Medical Information, Inc.)

Natriuretic peptides

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The relationship between cardiac charge movements associated with I (sub CA) and I (sub Na-Ca) in cardiac myocytes

Article Abstract:

A multitude of cellular events contribute to the normal contraction of heart muscle. Unfortunately, the events are so interrelated, it is difficult for physiologists to untangle the contribution of individual events. To examine the role of the sodium-calcium exchanger, an experiment was set up with special conditions. The muscle cells were given caffeine, which prevents the sarcoplasmic reticulum from reaccumulating calcium after releasing it during a contraction. The muscles cells were also placed in a medium without external sodium, so that the sodium-calcium exchanger would have no electrochemical power to pump calcium out of the cell. When the membrane voltage is clamped, the cells contract. However, the cells cannot relax, even after the membrane is returned to its normal voltage. The sarcoplasmic reticulum has released calcium, which is now stuck in the intracellular space with no place to go. A quick application of sodium ions on the outside of the cell, however, and the cell relaxes. The sodium has provided the electromotive force for the cell to pump out the excess sodium, and the cell relaxes. Calculations show that the sodium-calcium exchanger is capable of extruding all the calcium released into the intracellular space during cell contraction. (Consumer Summary produced by Reliance Medical Information, Inc.)

Heart, Heart contraction, Muscle cells

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