Augmentation by intracellular ATP of the delayed rectifier current independently of the glibenclamide-sensitive K-current in rabbit arterial myocytes.
Elevation of intracellular ATP levels by flash photolysis of caged ATP augmented the delayed rectifier K-current (IKDR) in rabbit pulmonary artery myocytes. The percentage augmentation was unaffected when IKDR was inactivated by 50% (holding potential -40 mV), although the magnitude of the ATP-induced current was substantially reduced. Inactivation of 90% IKDR (holding potential -20 mV) virtually abolished the ATP-dependent augmentation. We conclude that modulation of IKDR by ATP does not require conversion of the glibenclamide-sensitive K-current (IK(ATP)).
Department of Pharmacology, UMDS, St. Thomas's Hospital, London.
A M
AM
Evans
L H
LH
Clapp
A M
AM
Gurney
D000255:Adenosine Triphosphate / Q000494:pharmacology*; D000818:Animals; D005905:Glyburide / Q000494:pharmacology*; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D010766:Phosphorylation; D015221:Potassium Channels / Q000187:drug effects* / Q000502:physiology; D011651:Pulmonary Artery / Q000378:metabolism; D011817:Rabbits
D015221:Potassium Channels; D000255:Adenosine Triphosphate; D005905:Glyburide