Modulation of contractility in failing human myocytes by reverse-mode Na/Ca exchange

Valentino Piacentino, Christopher R. Weber, John P. Gaughan, Kenneth B. Margulies, Donald M Bers, Steven R. Houser

Research output: Contribution to journalArticlepeer-review

15 Scopus citations


A decrease in the peak systolic [Ca]i and slow decay of the Cai transient are common features of the end-stage failing human ventricular myocyte and may underlie the contractile abnormalities observed in congestive heart failure. The role of the Na/Ca exchanger has been a great area of interest given the changes observed at the molecular level. Results from these experiments have been inconsistent, however, and therefore cellular-based experiments may be required to characterize the role of the Na/Ca exchanger in failing human myocardium. We review recent data that suggest an increased ability of the Na/Ca exchanger to transport Ca into the cytoplasm in failing human myocytes. We hypothesize that this increased Ca influx can explain the slowed decay and impaired relaxation of failing human ventricular myocytes.

Original languageEnglish (US)
Pages (from-to)466-471
Number of pages6
JournalAnnals of the New York Academy of Sciences
StatePublished - 2002
Externally publishedYes


  • Cardiac Na/Ca exchange
  • Contractility
  • Heart failure
  • Sarcoplasmic reticulum

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)


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