SPONTANEOUS TRANSIENT OUTWARD CURRENTS AND DELAYED RECTIFIER K- EFFECTS OF HYPOXIA( CURRENT )

Single smooth muscle cells of rabbit intrapulmonary artery were voltag e 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 tetraethylammon ium sensitive and activated by Ca2+ influx, they were believed to repr esent activation of Ca2+-activated K+ channels. The steady-state outwa rd current, which was sensitive to 4-aminopyridine, was the delayed re ctifier K+ current. In cells voltage clamped at 0 mV, we found that ST OCs were not randomly distributed in amplitude but were composed of mu ltiples of 1.57 +/- 0.56 pA/pF. The mean frequency of STOCs was 5.51 /- 3.49 Hz. Ryanodine (10 mu M), caffeine (5 mM), thapsigargin (200 nM ), and hypoxia (Po-2 = 10 mmHg) decreased STOCs. The effect of hypoxia on STOCs was partially reversible only if the experiment was conducte d in the presence of thapsigargin. Hypoxia and thapsigargin decrease s teady-state outward current. Thapsigargin and removal of external Ca2 abolished the effect of hypoxia, suggesting that hypoxia decreases st eady-state outward current by a Ca2+-dependent mechanism.