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Effects of cromakalim on the membrane potassium permeability of frog skeletal muscle in vitro
Author(s) -
Benton D.C.,
Haylett D.G.
Publication year - 1992
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.1476-5381.1992.tb14478.x
Subject(s) - cromakalim , diazoxide , potassium channel , glibenclamide , tolbutamide , chemistry , skeletal muscle , phentolamine , medicine , muscle contraction , potassium channel opener , membrane potential , endocrinology , sartorius muscle , biophysics , pharmacology , biology , biochemistry , propranolol , insulin , diabetes mellitus
1 The effects of the potassium channel opener, cromakalim, and its active enantiomer, lemakalim, have been investigated in frog skeletal muscle. 2 Cromakalim (30–300 μ m ) increased 86 Rb efflux from muscles loaded with the isotope, hyperpolarized the fibres and reduced membrane resistance. 3 These effects were inhibited by the sulphonylureas, glibenclamide and tolbutamide. The IC 50 for glibenclamide inhibition of 86 Rb efflux was ca. 8 n m . 4 Phentolamine (300 μ m ) (which blocks responses to cromakalim in smooth muscle and inhibits ATP‐sensitive K + channels in pancreatic β‐cells) had no effect on the reduction in membrane resistance caused by 100 μ m lemakalim. 5 Diazoxide (600 μ m ) had no effect on 86 Rb efflux. 6 The similarities of the K + channel activated by cromakalim in frog skeletal muscle to the channel acted on in smooth muscle and to the ATP‐sensitive K + channel of β‐cells are discussed.