|
KMID : 0364019920250040347
|
|
Korean Journal of Thoracic and Cardiovascular Surgery
1992 Volume.25 No. 4 p.347 ~ p.355
|
|
|
Inhibitory effect of Mg2+ on the release of Ca2= from Ryanodine Receptor of the sarcoplasmic Reticulum in the skeletal Muscle
|
|
|
|
|
Abstract
|
|
|
The precise mechanism of the Excitation-Contraction Coupling is still uncertain. But the concept that Ca2+ induced Ca2+ release (CICR) from the Ryanodine receptor in the sarcoplasmic reticulm (Foot structure) may play a major role in E-C coupling
has
been widely accepted since 1970's. It is believed that increased cytosolic Ca2+ followed by CICR is main contributor for E-C coupling of striated muscle.
Resulting phenomena of ischemic/post-reperfusion myocyte is increased cytosolic Ca2+, even to the absence of Ca2+ in reperfusate. So intracellular inhibitor to CICR might prevent the ischemic and reperfusion damage of myocardial cells.
The relatively purified foot protein, especially heavy sarcoplasmic reticulum rich, of the skeletal muscle was incorporated into the black lipid bilayer (Phosphatidyl ethanolamine: Phosphatidyl serine=1 : 1). Under the steady state of membrane
potential
(+20mV), ionic current through Ryanodine receptor was measured with Cs+ as charge carrier. In the cis chamber (Cytoplasmic side), Mg2+ strongly inhibited CICR of Ryanodine receptor (Kd=6.2nM).
In conclusion, naturally existing intracellular free Mg2+ can inhibit CICR from intracellular Ca2+ reservior (heavy SR). So post-ischemic or post-reperfusing myocardium could be preserved using additional free Mg2+ in cardioplegic solution or
reperfusate, otherwise the optimal concentration is undetermined.
|
|
|
KEYWORD
|
|
|
|
|
|
FullTexts / Linksout information
|
|
 
|
|
|
Listed journal information
|
|
  
|