ArticleBritish journal of pharmacology1993
Induction of a glibenclamide-sensitive K-current by modification of a delayed rectifier channel in rat portal vein in insulinoma cells.
Article in British journal of pharmacology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Redox control of cardiac excitability.Antioxidants & redox signaling · 2013Review
- Antipyretic and antinociceptive effects of Nauclea latifolia root decoction and possible mechanisms of action.Pharmaceutical biology · 2011Article
- Thiazolidinone CFTR inhibitor identified by high-throughput screening blocks cholera toxin-induced intestinal fluid secretion.The Journal of clinical investigation · 2002Article
- Tolbutamide causes open channel blockade of cystic fibrosis transmembrane conductance regulator Cl- channels.Biophysical journal · 1996Article
- Potentiation of P1075-induced K+ channel opening by stimulation of adenylate cyclase in rat isolated aorta.British journal of pharmacology · 1995Article
- Pharmacology of the potassium channel openers.Cardiovascular drugs and therapy · 1995Review
- Inhibition of delayed rectifier K(+)-current by levcromakalim in single intestinal smooth muscle cells: effects of cations and dependence on K(+)-flux.British journal of pharmacology · 1995Article
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Authors and funding
2 authors.
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Abstract
In insulinoma cells (RINm5F), the glibenclamide-sensitive K-current (IK(ATP)) which developed spontaneously or after exposure to levcromakalim or to butanedione monoxime was always accompanied by a reduction in the delayed rectifier current (IK(V)). At potentials over which IK(V) was fully activated, the total outward current remained constant. In rat portal vein, the delayed rectifier channel inhibitor, margatoxin, reduced the combined induction of IK(ATP) and inhibition of IK(V) by levcromakalim. These data suggest that the ATP-sensitive K-channel, K(ATP), is a voltage-insensitive state of the delayed rectifier, KV.
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