Key result
Hypoxia inhibited the Ca2+-insensitive component of the delayed voltage-activated outward K+ current and caused depolarization only after an initial priming depolarization in rat pulmonary myocytes.
Population
Myocytes isolated from rat small pulmonary arteries
Comparison
Hypoxia (PO2, 20-30 mmHg) vs Baseline/normoxic conditions
Design
Preclinical
Authors
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Questions control of resting membrane potential by delayed rectifier K+ channels in pulmonary myocytes; hypothesis-generating for hypoxic vasoconstriction mechanisms.
In rat pulmonary arterial myocytes, hypoxia inhibits delayed rectifier K+ channels only after an initial priming depolarization, indicating they do not control resting membrane potential.
Turner et al. (1997) studied this question. Hypoxia was evaluated on Voltage-activated K+ currents and membrane potential. Hypoxia inhibited the Ca2+-insensitive component of the delayed voltage-activated outward K+ current and caused depolarization only after an initial priming depolarization in rat pulmonary myocytes.
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