ACTIVATION OF ATP-DEPENDENT K-MUSCLE CELLS ISOLATED FROM THE PIG CORONARY-ARTERY( CHANNELS BY HYPOXIA IN SMOOTH)

1. The perforated patch technique with amphotericin B was used to reco rd whole-cell currents activated by hypoxia in smooth muscle cells, is olated enzymatically from pig coronary arteries. 2. Superfusion with h ypoxic solution (O-2 partial pressure, 25-40 mmHg) activated an inward current at -60 mV in 143 mM extracellular K+. The reversal potential of the current induced by hypoxia shifted with extracellular [K+] as e xpected for a K+ current, while its current-voltage relation was consi stent with the channels showing little voltage dependence. 3. The hypo xia-induced current was inhibited by glibenclamide (10 mu M), but was unaffected by charybdotoxin (50 nM). 4. In whole-cell recordings at -6 0 mV in 143 mM K+ solution, openings of single channels passing a curr ent close to -2 pA could sometimes be detected in normoxic solution. O penings became more frequent during the onset of the response to hypox ia, when several levels could be detected. Channels with a similar con ductance were activated by hypoxia in cell-attached patches. 5. Our re sults suggest that hypoxia activates ATP-dependent K+ channels. We dis cuss possible mechanisms by which this activation may occur.