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1 Justus Liebig University, 35392 Giessen, Germany; and 2 Veterans Affairs Medical Center, University of Minnesota, Minneapolis, Minnesota 55417
Many studies indicate that hypoxic
inhibition of some K+ channels in the membrane of the
pulmonary arterial smooth muscle cells (PASMCs) plays a part in
initiating hypoxic pulmonary vasoconstriction. The sensitivity of the
K+ current (Ik), resting membrane
potential (Em), and intracellular Ca2+ concentration ([Ca2+]i) of
PASMCs to different levels of hypoxia in these cells has not been
explored fully. Reducing PO2 levels gradually
inhibited steady-state Ik of rat resistance
PASMCs and depolarized the cell membrane. The block of
Ik by hypoxia was voltage dependent in that low
O2 tensions (3 and 0% O2) inhibited
Ik more at 0 and 
20 mV than at 50 mV. As
expected, the hypoxia-sensitive Ik was also
4-aminopyridine sensitive. Fura 2-loaded PASMCs showed a graded
increase in [Ca2+]i as
PO2 levels declined. This increase was reduced
markedly by nifedipine and removal of extracellular Ca2+.
We conclude that, as in the carotid body type I cells, PC-12 pheochromocytoma cells, and cortical neurons, increasing severity of
hypoxia causes a proportional decrease in Ik and
Em and an increase of
[Ca2+]i.
hypoxic pulmonary vasoconstriction; patch clamp; electrophysiology; ion channels; oxygen
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