Abstract. Developmental changes in excitation-contraction mechanisms were examined in the ventricular myocardium from fetal, neonatal, and 1-, 2-, and 4-week-old mice. In isolated tissue, the negative inotropic effect of nifedipine decreased, while that of ryanodine increased with age. Action potential duration decreased with age, especially during the late fetal period. In ventricular cardiomyocytes, fluorescence imaging revealed that the sarcoplasmic reticulum increases progressively during pre-and postnatal development. t-Tubules were absent in the fetus and neonate, were observed only in the subsarcolemmal region at 1 week after birth, and were present throughout the cytoplasm at 2 and 4 weeks after birth. The amplitude of Ca 2+ transients, as well as its ryanodine-sensitive component, increased with age. In the neonate and 1-week-old mice, Ca 2+ at the cell center showed slower rise than the subsarcolemmal region, but in 2-and 4-week-old mice, Ca 2+ increased simultaneously across the entire width of the cell. These results suggest that in the mouse ventricular myocardium, the shortening of the action potential during the late fetal period and the development of t-tubule-sarcoplasmic reticulum coupling during the second postnatal week largely contribute to the developmental increase in the dependence of contraction on sarcoplasmic reticulum function.

Abstract. We recorded the electrical activity from the myocardial layer of isolated mouse pulmonary veins with the glass microelectrode technique. Spontaneous electrical activity was observed in about half of the preparations, which appeared either as constant firing or as repetitive bursts. Noradrenaline enhanced, while acetylcholine reduced, automatic activity. The action potentials evoked in quiescent preparations showed a resting membrane potential less negative than the atria and an extremely rapid early repolarization followed by a late plateau. The present study revealed that the mouse pulmonary vein myocardium shows diverse electrical activity, which is influenced by autonomic neurotransmitters.

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