DA closure is essential to the hemodynamic transition from fetus to neonate. We studied K+ channel activity (IK) in preterm and term DAs, using perforated-patch-clamp techniques. Freshly isolated smooth muscle cells were obtained from fetal rabbit pups at 24 and 31 days gestation (term=31 days). All recordings were made in hypoxia (PaO2=25mmHg) at 32°C. At positive potentials, IK was inhibited by tetraethylammonium (TEA; 5mM: Ca2+-dependent K+ channel (KCa) blocker) and 4-aminopyridine (4-AP; 1mM; delayed rectifier (KDR) blocker) independent of DA age. However. IK recorded around the resting membrane potential (∼-50mV) was only inhibited by TEA in preterm cells and 4AP in term cells (n=8). Cells from preterm pups depolarized on exposure to TEA (n=5), while cells from term DAs depolarized to 4AP (n=5). IK recorded from term, but not preterm. DAs was inhibited by normoxia (n=5) We suggest that during development, the K+ channel controlling DA resting membrane potential, changes from KCa to the O2-sensitive KDR (J. Clin. Invest. 98: 1959-1965 1996). This switch in K+ channel expression may determine the stage at which the DA constricts to O2.
|Original language||English (US)|
|State||Published - Dec 1 1997|