Calcium transport by intracellular membrane structures in the myocardium of hypertrophied and failing hearts

Cor Vasa. 1986;28(5):373-83.

Abstract

After inducing haemodynamic cardiac overload in rabbits, the authors studied in several stages (1-14 months) the calcium transport activity of the mitochondrial and sarcoplasmic myocardial fractions using labelled 45CaCl2. A coincidence was found between changes in myocardial contractility and changes in calcium transport activity of intracellular organelles. A possible important role of mitochondria in this adaptive process was also documented. Since the calcium transport capacity of the sarcoplasmic reticulum progressively decreases (with the exception of the earliest stages following overload induction), it seems that increased myocardial contractility ensures enhanced Ca transport activity of the mitochondria. Myocardial contractility drops only at the time when the Ca transport activity of the mitochondria decreases. Since these changes occur already at the time of regression of myocardial hypertrophy, which precedes heart failure, it can be assumed that they are causally connected with the reduced contractility of a failing heart.

MeSH terms

  • Animals
  • Antimycin A / analogs & derivatives
  • Antimycin A / pharmacology
  • Calcium / metabolism*
  • Calcium-Transporting ATPases / metabolism
  • Cardiomegaly / metabolism*
  • Chemical Fractionation
  • Heart Failure / metabolism*
  • Intracellular Membranes / metabolism*
  • Mitochondria, Heart / metabolism
  • Myocardium / metabolism*
  • Oligomycins / pharmacology
  • Rabbits
  • Rotenone / pharmacology
  • Sarcoplasmic Reticulum / metabolism

Substances

  • Oligomycins
  • Rotenone
  • antimycin
  • Antimycin A
  • Calcium-Transporting ATPases
  • Calcium