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10.1007/BF00239537

http://scihub22266oqcxt.onion/10.1007/BF00239537
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1770948!ä!1770948

suck abstract from ncbi


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pmid1770948      Mol+Cell+Biochem 1991 ; 108 (1): 9-17
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  • Impaired calcium uptake by cardiac sarcoplasmic reticulum and its underlying mechanism in endotoxin shock #MMPMID1770948
  • Wu LL; Liu MS
  • Mol Cell Biochem 1991[Nov]; 108 (1): 9-17 PMID1770948show ga
  • Effects of endotoxin administration on the ATP-dependent Ca2+ uptake by canine cardiac sarcoplasmic reticulum (SR) were investigated. Results obtained 4 h after endotoxin administration show that ATP-dependent Ca2+ uptake by cardiac SR was decreased by 27-43% (p less than 0.05). Kinetic analysis indicates that the Vmax values for Ca2+ and for ATP were significantly decreased while the S0.5 and the Hill coefficient values were not affected during endotoxin shock. Magnesium (1-5 mM) stimulated while vanadate (25-250 microM) inhibited the ATP-dependent Ca2+ uptake, but the Mg(2+)-stimulated and the vanadate-inhibited activities remained significantly lower in the endotoxin-treated animals. Phosphorylation of SR by the exogenously added catalytic subunit of the cAMP-dependent protein kinase or by the addition of calmodulin stimulated the ATP-dependent Ca2+ uptake activities both in the control and endotoxin-injected dogs. However, the phosphorylation-stimulated activities remained significantly lower in the endotoxin-injected dogs. Dephosphorylation of SR decreased the ATP-dependent Ca2+ uptake, but the half-time required for the maximal dephosphorylation was reduced by 31% (p less than 0.05) 4 h post-endotoxin. These data indicate that endotoxin administration impairs the ATP-dependent Ca2+ uptake in canine cardiac SR and the endotoxin-induced impairment in the SR calcium transport is associated with a mechanism involving a defective phosphorylation and an accelerated dephosphorylation of SR membrane protein. Since ATP-dependent Ca2+ uptake by cardiac SR plays an important role in the regulation of the homeostatic levels of the contractile calcium, our findings may provide a biochemical explanation for myocardial dysfunction that occurs during endotoxin shock.
  • |Adenosine Triphosphate/*metabolism[MESH]
  • |Animals[MESH]
  • |Calcium/*metabolism[MESH]
  • |Dogs[MESH]
  • |Endotoxins/*toxicity[MESH]
  • |Kinetics[MESH]
  • |Magnesium/pharmacology[MESH]
  • |Male[MESH]
  • |Phosphorylation[MESH]
  • |Sarcoplasmic Reticulum/*metabolism[MESH]
  • |Shock, Septic/*metabolism[MESH]


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