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KMID : 0371919890020010001
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Journal of Wonju College of Medicine
1989 Volume.2 No. 1 p.1 ~ p.8
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The Origin and Action Mechanism of Ca^(++) Ion in Myocardial Contraction
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Abstract
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Calcium is an important second messenger to trigger a lot of intracellular processes. Myocardial contraction is one of such processes triggered by intracellular free calcium. Previoulsly slow inward calcium current through calcium channel was believed to be the main route of calcium entry for myocardial contraction. But recently, many evidences were reported there may be other calcium entry routes than slow calcium channel. Among them, the Na^(+)-Ca^(++) exchange is the most widely accepted mechanism as another calcium entry. So, present study was performed to identify the role of Na^(+)-Ca^(++) exchange in myocardial contraction. We used left atrium of Sprague Dawley rat of either sex. Atrial contraction was induced by electrical field stimulation (0.5 msec, 2 ㎐, 10 volts) through platinum electrodes. By changing the stimulating frequency from 2 ㎐ to 0.2 ㎐ and 0.2 ㎐ to 2 ㎐, the changes of atrial contractile force was monitored. The results were as follows;
1. By decreasing the frequency from 2 ㎐ to 0.2 ㎐, the contractile force of rat left atrium was increased and maintained more than 5 minutes. Just after returning the frequency rate from 0.2 ㎐ to 2 ㎐, contractile force was rapidly decreased and then slowly increased to normal contraction.
2. Norepinephrine treatment reversed the changes of contractile tension. So, the contractile tension was rather increased just after returning the stimulating frequency from 0.2 ㎐ to 2 ㎐.
3. Tetrodotoxin treatment decreased the contractile force of rat atrium and abolished the tension increase after returning the stimulating frequency from 0.2 ㎐ to 2 ㎐.
4. Verapamil treatment almost completely suppressed the contractility of rat atrium. But never abolished the tension increase after changing the frequency from 2 ㎐ to 0.2 ㎐.
5. By combined treatment of tetrodotoxin and verapamil, the tension increase by changing the frequency from 2 ㎐ to 0.2 ㎐ was far suppressed than verapamil alone. From these above results, it was suggested that Na^(+)-Ca^(++) exchange may play an important role in myocardial contraction in addition to calcium entry through slow calcium channel.
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