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KMID : 0357220070190050065
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Journal of Korean Society Physical Therapy
2007 Volume.19 No. 5 p.65 ~ p.76
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The Relationship of the L-type Ca²+ Channel on the Depolarization-and Depletion of SR Ca²+ -induced Smooth Muscle Contraction and Intracellular Ca²+ Mobilization
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Kim Jung-Hwan
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Abstract
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Purpose: It is generally accepted that smooth muscle contraction is triggered by intracellular () released from intracellular stores such as sarcoplasmic teticulum (SR) and from the extracellular space. The increased can phosphorylate the 20,000 dalton myosin light chain by activating MLC kinase (MLCK), and this initiates smooth muscle contraction. In addition to the MACK-tension pathway, a number of intracellular signal molecules, including mitogen-activated protein kinase (MAPK), protein kinase C (PKC) and others, play important roles in the regulation of smooth muscle contraction. However, the mechanisms regulating contraction of depletion of SR in mouse gastric smooth muscle strips is not still clear.
Methods: To investigate the rotes of influx and SR release channel on gastric motility, isometric contraction and were examined in mouse gastric smooth muscle strips.
Results: High KCl, ryanodine, an activator of induced release channel, and cyclopiazonic acid (CPA), an inhibitor of SR ATPase evoked a sustained increase in muscle contraction and . These increases induced by high KCl, ryanodine, and CPA were partially blocked by application of verapamil (), a L-type channel inhibitor. Additionally, in free solution (1 mM EGTA), ryanodine and CPA had no effect contraction and in fundic muscle strips.
Conclusion: These results that extracellular influx and depletion of SR trigger influx through verapamil-sensitive channel, and extracellular and SR store may functionally involve in the subcellular mobilization in mouse gastric muscle.
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KEYWORD
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Smooth Muscle Contraction, Intracellular Ca²+Ca²+ Influx and Release
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