Key result
The resting potential of rabbit pulmonary artery myocytes depends on a low threshold, non-inactivating K+ current (IK(N)), and its inhibition by hypoxia mediates membrane depolarization.
Population
Rabbit isolated pulmonary artery myocytes
Comparison
Hypoxia, 4-aminopyridine (4-AP), and quinine vs Normoxic conditions / baseline
Design
Preclinical
Authors
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May inform hypoxic pulmonary vasoconstriction mechanisms in rabbits; leaves open relevance to human disease.
The resting potential of rabbit pulmonary artery myocytes depends on a low threshold, non-inactivating K+ current (IK(N)), whose inhibition may mediate hypoxia-induced depolarization.
Osipenko et al. (1997) studied Hypoxia-induced depolarization. Hypoxia and potassium channel blockers (4-AP, quinine) vs. Baseline/Normoxia was evaluated on Resting membrane potential and potassium currents (IK(N), IK(V), IK(A)). The resting potential of rabbit pulmonary artery myocytes depends on a low threshold, non-inactivating K+ current (IK(N)), and its inhibition by hypoxia mediates membrane depolarization.
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