Hormonal control of Mg2+ transport in the heart
Article Abstract:
Magnesium is the second most abundant cation, or positively charged ion, within cells. The closely related cation, calcium, serves as a messenger within the cell, and changes in local calcium concentration can trigger important cellular events. It is unlikely, however, that magnesium ions can serve a similar function. Since most of the magnesium ions are floating free within the cell, it would be difficult to obtain the rapid local changes in concentration necessary to control the cellular machinery. However, changes in the total magnesium concentration do exert a variety of effects on cellular physiology. Important metabolic pathways, mitochondrial ion transport, and the activity of some calcium channels are among the cellular processes which are influenced by magnesium concentration. Although the concentration of magnesium may be experimentally varied, little is known about how the cells might regulate their own magnesium concentration under natural conditions. It has currently been observed that heart cells alter their internal magnesium concentration in response to noradrenaline. The phenomenon, which results from the stimulation of beta-adrenergic receptors at the cell surface and the subsequent increase in cyclic adenosine monophosphate (a nucleotide that is involved in a wide variety of metabolic responses to cell stimuli) concentration, has been observed both in isolated heart muscle cells and in cells of the intact heart. In response to noradrenaline, magnesium begins to move out of the heart cells. The effect is considerable; about 20 percent of the total magnesium moves out of the heart within a few minutes. The exact mechanism by which this is accomplished is not yet clear. Since the concentration of magnesium within the cells is greater than that outside the cells, it is possible that the magnesium simply leaks out. However, it seems more likely that an alteration in the pumping mechanism may result in both greater leakage and decreased transport back into the cell. While the role that this alteration in magnesium concentration might play in normal heart physiology is not certain, it may represent another mechanism by which noradrenaline can modulate heart function. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 1990
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Kinetics, stoichiometry, and role of the Na-Ca exchange mechanism in isolated cardiac myocytes
Article Abstract:
The concentration of calcium ions within heart muscle cells play a critical role in stimulating the contraction of these cells during the heartbeat. However, the intracellular concentration of calcium ions is affected by many factors, which makes their study a challenge for physiologists. It has been known for some time that there is an exchange pump in the heart cell membrane (sarcolemma). This pump is called an exchange pump; calcium is pumped out of the cell as sodium ions flow in. The ratio of sodium to calcium ions seems to be a constant three to one. Although the contraction of the heart cells is clearly stimulated by a transient increase in calcium, it is uncertain to what degree the sodium-calcium exchange pump contributes to this process. Fortunately, the calcium concentration in cells may be directly measured using special fluorescent dyes such as indo-1. These dyes change their fluorescent properties in response to changes in the local calcium concentration. When these dyes are injected into living cells, a specially equipped microscope can monitor changes in the calcium. The investigators used the heart drug verapamil to block the calcium channels in the cell membrane, and the drug ryanodine to inhibit the sarcoplasmic reticulum from sequestering calcium within the cell. Thus, they were assured that any changes observed would be due to the sodium-calcium exchange pump. The results showed that the pump is too slow to play the major role in the muscle contraction. A transient rise in calcium stimulates the contraction, and only 15 percent of the reduction that follows can be accounted for by the action of the exchange pump. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 1990
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A new wave for heart rhythms
Article Abstract:
The coexpression of K(sub v)LQT1 and IsK, results in a slowly activating delayed-rectifier K+ current with gating current similar to that of native cardiac slow delayed-rectifier current (I(sub Ks)). K(sub v)LQT1 and IsK are the two components, governing I(sub Ks). KVLQT1 gene encodes a K+ channel, and IsK is a type-III glycoprotein. The expression of K(sub v)LQT1 or IsK alone does not cause current similar to the native K+ currents. The positive regulation of I(sub Ks) by drugs may be helpful in arrhythmia. A better understanding of K(sub v)LQT1/IsK complex may help drug designing.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 1996
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