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Division of Pulmonary and Critical Care Medicine, Department of Medicine, The Johns Hopkins University, Baltimore, Maryland 21224
We tested the
hypothesis that chronic hypoxia alters the regulation of
K+ channels in intrapulmonary
arterial smooth muscle cells (PASMCs). Charybdotoxin-insensitive,
4-aminopyridine-sensitive voltage-gated K+
(KV,CI) and
Ca2+-activated
K+
(KCa) currents were measured in
freshly isolated PASMCs from rats exposed to 21 or 10%
O2 for 17-21 days. In
chronically hypoxic PASMCs, KV,CI
current was reduced and KCa
current was enhanced. 4-Aminopyridine (10 mM) depolarized both normoxic
and chronically hypoxic PASMCs, whereas charybdotoxin (100 nM) had no
effect in either group. The inhibitory effect of endothelin (ET)-1
(10
7 M) on
KV,CI current was significantly
reduced in PASMCs from chronically hypoxic rats, whereas inhibition by
angiotensin (ANG) II (107
M) was enhanced. Neither ET-1 nor ANG II altered
KCa current in normoxic PASMCs;
however, both stimulated KCa
current at positive potentials in chronically hypoxic PASMCs. These
results suggest that although modulation of
KV,CI and
KCa channels by ET-1 and ANG II is
altered by chronic hypoxia, the role of these channels in the
regulation of resting membrane potential was not changed.
voltage-gated potassium current; calcium-activated potassium current; membrane potential
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