Maturation of the heart.

The transition from fetal to newborn to adult previously has been associated with a progressive increase in myocardial contractile function. The purpose of this review is to summarize new information on the biochemical and molecular processes that regulate the perinatal maturation of heart function. The developing heart experiences a perinatal increase in the cellular quantity of the sarcoplasmic reticulum and the myofibrils, the organelles that regulate and utilize cytosolic calcium to produce cardiac contraction. It also has become evident that the function of the available ion pump proteins is reduced in fetuses and newborns compared to adults of the same species. The resultant limited regulation of cytosolic calcium concentrations by the sarcoplasmic reticulum enhances the role of the sarcolemma in this process. Although it appears that the perinatal maturation of sarcoplasmic reticular function is not under direct molecular regulation, alternative splicing may regulate its gene products. A great deal of the perinatal maturation of myofibrillar protein function appears to be regulated by molecular processes. This has been best demonstrated in detail for myosin. In some species, such as the rat, much of the perinatal increase in myocardial contractile function can be explained by a parallel change in myosin isoforms. This isoform shift alters the activity of its ion pump, thereby allowing it to utilize more calcium. In contrast, the perinatal maturation of contractile function in several larger species cannot be explained fully by the extent of the molecular changes that have been identified currently in these species.