Postnatal development in rat ventricular myocytes is associated with an increase in IK1 current, which may explain the developmental shortening of the action potential.
The neonatal rat ventricular action potential has a shape similar to that of most adult mammals. However, shortly after birth, the action potential shortens to a spike-like configuration. The contribution of changes in repolarizing currents to the shortening is unclear. Thus the inwardly rectifying potassium current (IK1) was measured in heart cells from rats of varying ages using patch-clamp techniques. In freshly isolated cells, whole cell IK1 currents increased greatly between ages 3 and 9-13 days and remained constant thereafter. In culture, IK1 disappeared preferentially in older cells, obscuring the developmental increase. Age-dependent differences in single-channel activity were also observed. Adult cells had IK1 channels consisting of two populations (30 and 42 pS), whereas neonatal cells exhibited only the lower conductance channel. The appearance of the 42-pS channel may contribute a part of the developmental increase in IK1. It was concluded that IK1 increases during postnatal development of the rat ventricle and that this increase may contribute to the postnatal shortening of the rat ventricular action potential.
Gordon M. Wahler (1992) studied this question.