Premium
Activation of ATP‐dependent K+ channels by hypoxia in smooth muscle cells isolated from the pig coronary artery.
Author(s) -
Dart C,
Standen N B
Publication year - 1995
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1995.sp020565
Subject(s) - charybdotoxin , hypoxia (environmental) , glibenclamide , extracellular , biophysics , reversal potential , chemistry , electrophysiology , patch clamp , membrane potential , medicine , anatomy , biology , endocrinology , oxygen , biochemistry , organic chemistry , diabetes mellitus
1. The perforated patch technique with amphotericin B was used to record whole‐cell currents activated by hypoxia in smooth muscle cells, isolated enzymatically from pig coronary arteries. 2. Superfusion with hypoxic solution (O2 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 expected for a K+ current, while its current‐voltage relation was consistent with the channels showing little voltage dependence. 3. The hypoxia‐induced current was inhibited by glibenclamide (10 microM), but was unaffected by charybdotoxin (50 nM). 4. In whole‐cell recordings at ‐60 mV in 143 mM K+ solution, openings of single channels passing a current close to ‐2 pA could sometimes be detected in normoxic solution. Openings became more frequent during the onset of the response to hypoxia, when several levels could be detected. Channels with a similar conductance were activated by hypoxia in cell‐attached patches. 5. Our results suggest that hypoxia activates ATP‐dependent K+ channels. We discuss possible mechanisms by which this activation may occur.