INWARDLY RECTIFYING POTASSIUM CURRENT IN RAT FETAL AND NEONATAL VENTRICULAR CARDIOMYOCYTES

Citation
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
Citations number
16
Categorie Soggetti
Physiology
ISSN journal
00029513
Volume
265
Issue
4
Year of publication
1993
Part
2
Pages
80001107 - 80001111
Database
ISI
SICI code
0002-9513(1993)265:4<80001107:IRPCIR>2.0.ZU;2-8
Abstract
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.