Regulation by glucose availability of tension development and electrical activity in fetal and neonatal rat hearts.

The aim of the present article was to study if changes in glucose availability modify the functional activity of the glucose-dependent developing heart. Our data indicate that a decrease in glucose availability increases tension development and action potential duration at early fetal stages. This fact could probably be explained by the enhancement of Ca2+ movements that regulate the number and turnover rate of membrane glucose transporters in muscle cells. The sensitivity to glucose availability decreases postnatally as the heart becomes fatty acid-dependent.