We studied the mechanisms regulating contractions in first trimester human fetal hearts. We hypothesized calcium influx through the calcium channels is the dominant mechanism for contractions, and calcium efflux through sodium-calcium exchange is important for relaxation early in developing human hearts. To test our hypothesis, we studied contractions in cultured cardiac myocyte clusters, and electron micrographs from first trimester fetal hearts obtained under the guidelines of an approved human use protocol (UUMC IRB#5754-96). When we perfused 8 clusters of cells with 10 μM ryanodine to inhibit the sarcoplasmic reticulum, contractions did not change significantly (95±3.2% of baseline). When we perfused 8 clusters of cells with 20 μM nifedipine to inhibit calcium channel influx, contractions were eliminated. When we perfused 5 clusters of cells with 0 mM external sodium to inhibit sodium-calcium exchange, relaxation was prolonged and the resting baseline rose in 2. Electron micrographs from 5 first trimester hearts demonstrated 1 or rarely 2 rows of myofibrils in the subsarcolemmal regions of the ventricular myocytes with indistinct A and 1 bands. T-tubules and sarcoplasmic reticulum were not seen. Thus, the sarcoplasmic reticulum does not contribute to contractions in first trimester human fetal hearts. Calcium influx through the calcium channels is the dominant mechanism for contractions, and sodium-calcium exchange is important for relaxation.
|Original language||English (US)|
|State||Published - 1997|
All Science Journal Classification (ASJC) codes
- Molecular Biology