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Ca2+ uptake by cardiac sarcoplasmic reticulum from patients with idiopathic dilated cardiomyopathy

M A Movsesian1, M R Bristow, J Krall

  • 1Cardiology Division, University of Utah Medical Center, Salt Lake City 84108.

Circulation Research
|October 1, 1989
PubMed

Insights

Calcium handling in human hearts with dilated cardiomyopathy is not due to sarcoplasmic reticulum issues. This study found normal calcium uptake in failing hearts, suggesting other mechanisms are at play.

Area of Science:

  • Cardiovascular Physiology
  • Molecular Cardiology
  • Biochemistry

Background:

  • Idiopathic dilated cardiomyopathy (IDCM) is a significant cause of heart failure in humans.
  • Abnormal calcium (Ca2+) handling is implicated in the pathophysiology of heart failure.
  • Sarcoplasmic reticulum (SR) plays a crucial role in regulating intracellular Ca2+ concentrations.

Purpose of the Study:

  • To investigate the intrinsic Ca2+ uptake function of the sarcoplasmic reticulum in human hearts with IDCM.
  • To compare Ca2+ uptake kinetics and beta-receptor density in failing versus nonfailing human ventricular myocardium.

Main Methods:

  • Preparation of sarcoplasmic reticulum from left ventricular myocardium of nonfailing and IDCM (Class IV) human hearts.
  • Measurement of Ca2+ uptake kinetics (Vmax, K0.5, nHill) by sarcoplasmic reticulum.
  • Quantification of beta-receptor density in crude sarcolemma.

Main Results:

  • Ca2+ uptake by sarcoplasmic reticulum showed no significant difference between nonfailing (Vmax: 593 +/- 82 nmol/mg-min) and failing hearts (Vmax: 593 +/- 36 nmol/mg-min).
  • Kinetic parameters (K0.5 and nHill) for Ca2+ uptake were similar in both groups.
  • Beta-receptor density was significantly lower in failing hearts (52.1 +/- 4.5 fmol/mg) compared to nonfailing donors (110.0 +/- 15.3 fmol/mg).

Conclusions:

  • Intrinsic Ca2+ uptake by sarcoplasmic reticulum is not impaired in human idiopathic dilated cardiomyopathy.
  • Abnormal Ca2+ handling in IDCM likely results from mechanisms other than intrinsic sarcoplasmic reticulum Ca2+ uptake dysfunction.
  • Reduced beta-receptor density in failing hearts may contribute to altered cardiac function.

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