Lh. Xie et al., DEVELOPMENT OF INWARDLY RECTIFYING K+ CHANNEL FAMILY IN RAT VENTRICULAR MYOCYTES, American journal of physiology. Heart and circulatory physiology, 41(4), 1997, pp. 1741-1750
The ATP-sensitive K+ current (I-K,I-ATP), the inward rectifier K+ curr
ent (I-K1), and the acetylcholine-activated K+ current (I-K,I-ACh) wer
e recorded in fetal, neonatal, and adult rat ventricular myocytes usin
g the patch-clamp technique. The density (pA/pF) of I-K1 increased fro
m gestation day 10 through neonatal day 1 and then decreased after neo
natal day 30. The density of I-K,I-ATP activated maximally by metaboli
c inhibition changed in parallel with the I-K1 density, and the densit
y of I-K,I-ATP channel distribution was 1.3 times higher than that of
I-K1 throughout the development. We failed to observe developmental ch
anges in the single-channel conductance and the mean open time of I-K1
and I-K,I-ATP channels. However, the open probability of the I-K,I-AT
P channel was lower in fetuses, and the sensitivity to ATP was highest
in 1-day neonates. I-K,I-ACh were present in the ventricle at all sta
ges of development but at a much lower density than in atrium. The rel
ationship between the resting membrane potential and the development o
f the inwardly rectifying K+ channel family is discussed.