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Am J Physiol Lung Cell Mol Physiol 275: L145-L154, 1998;
1040-0605/98 $5.00
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Vol. 275, Issue 1, L145-L154, July 1998

Spontaneous transient outward currents and delayed rectifier K+ current: effects of hypoxia

C. Vandier1, M. Delpech2, and P. Bonnet2

1 Unité Mixte de Recherche (UMR) Centre National de la Recherche Scientifique 6542, Physiologie des Cellules Cardiaques et Vasculaires, Faculté des Sciences, 37200 Tours Cedex; and 2 UMR Centre National de la Recherche Scientifique 6542, Physiologie des Cellules Cardiaques et Vasculaires, Faculté de Médecine, 37032 Tours Cedex, France

Single smooth muscle cells of rabbit intrapulmonary artery were voltage clamped using the perforated-patch configuration of the patch-clamp technique. We observed spontaneous transient outward currents (STOCs) and a steady-state outward current. Because STOCs were tetraethylammonium sensitive and activated by Ca2+ influx, they were believed to represent activation of Ca2+-activated K+ channels. The steady-state outward current, which was sensitive to 4-aminopyridine, was the delayed rectifier K+ current. In cells voltage clamped at 0 mV, we found that STOCs were not randomly distributed in amplitude but were composed of multiples of 1.57 ± 0.56 pA/pF. The mean frequency of STOCs was 5.51 ± 3.49 Hz. Ryanodine (10 µM), caffeine (5 mM), thapsigargin (200 nM), and hypoxia (PO2 = 10 mmHg) decreased STOCs. The effect of hypoxia on STOCs was partially reversible only if the experiment was conducted in the presence of thapsigargin. Hypoxia and thapsigargin decrease steady-state outward current. Thapsigargin and removal of external Ca2+ abolished the effect of hypoxia, suggesting that hypoxia decreases steady-state outward current by a Ca2+-dependent mechanism.

pulmonary artery smooth muscle cells; calcium ion regulation; sarcoplasmic reticulum; potassium ion


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