H. Masuda et N. Sperelakis, INWARDLY RECTIFYING POTASSIUM CURRENT IN RAT FETAL AND NEONATAL VENTRICULAR CARDIOMYOCYTES, The American journal of physiology, 265(4), 1993, pp. 80001107-80001111
Whole cell and single-channel inwardly rectifying potassium currents (
I(K1)) of freshly isolated single fetal (12 and 18 days) and neonatal
(1, 5, and 10 days) rat ventricular myocytes were recorded using patch
-clamp techniques. Whole cell I(K1) was elicited by hyperpolarizing te
st pulses from a holding potential of -40 mV. I(K1) densities increase
d markedly during heart development between fetal day 12 and until neo
natal day 5; there was no further increase on neonatal day 10. Cell-at
tached patch recordings of single I(K1) channels were employed with 15
0 mM K+ both in the pipette and bath solutions. Large-conductance (31
pS) K+ channels with short openings were observed both in fetal day 18
and neonatal day 5 but not in fetal day 12 cells. Only small-conducta
nce (11 pS) channels with long openings were observed in approximately
10% of the cells on fetal day 12. The open probability of the large-c
onductance channels was 2.6-fold greater on neonatal day 5 than on fet
al day 18. In conclusion, the increase in the I(K1) density during obs
erved heart development may be primarily due to an increase in the ope
n probability of the I(K1) channels, rather than to an increase in the
ir number. We suggest that the small-conductance channel infrequently
observed on fetal day 12 could be an immature type of I(K1) channel, w
hich disappears during development.