Abstract
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 language | English (US) |
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Pages (from-to) | 466-471 |
Number of pages | 6 |
Journal | Annals of the New York Academy of Sciences |
Volume | 976 |
State | Published - 2002 |
Externally published | Yes |
Keywords
- Cardiac Na/Ca exchange
- Contractility
- Heart failure
- Sarcoplasmic reticulum
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)