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Augmentation by intracellular ATP of the delayed rectifier current independently of the glibenclamide‐sensitive K‐current in rabbit arterial myocytes
Author(s) -
Evans A.M.,
Clapp L.H.,
Gurney A.M.
Publication year - 1994
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1994.tb14836.x
Subject(s) - glibenclamide , chemistry , intracellular , medicine , endocrinology , biophysics , myocyte , current (fluid) , biology , biochemistry , engineering , electrical engineering , diabetes mellitus
Elevation of intracellular ATP levels by flash photolysis of caged ATP augmented the delayed rectifier K‐current ( I KDR ) in rabbit pulmonary artery myocytes. The percentage augmentation was unaffected when I KDR was inactivated by 50% (holding potential − 40 mV), although the magnitude of the ATP‐induced current was substantially reduced. Inactivation of 90% I KDR (holding potential − 20 mV) virtually abolished the ATP‐dependent augmentation. We conclude that modulation of I KDR by ATP does not require conversion of the glibenclamide‐sensitive K‐current ( I KDR(ATP ).