Abstract
We have cloned a delayed rectifier type K channel from rat heart (RH1). RH1 was identical to the rat brain K channel BK2 and differed from recently cloned rat cardiac K channel RAK by one amino acid residue. Endothelin receptors(ETRs)-mediated modulation of RH1 current (IRH1) was studied using Xenopus oocyte expression system. Activation of two different subtypes of ETRs by endothelin-1 equally suppressed the amplitude of IRH1. Stimulation of phosphatidylinositol turnover will probably be responsible for the suppression.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cloning, Molecular
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DNA / genetics
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Endothelins / pharmacology*
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Evoked Potentials / drug effects
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Female
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Genetic Vectors
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Heart / physiology*
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Male
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Membrane Potentials / drug effects
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Oocytes / drug effects
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Oocytes / physiology
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Phosphatidylinositols / metabolism
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Potassium Channels / drug effects
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Potassium Channels / genetics*
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Potassium Channels / physiology*
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RNA, Messenger / genetics
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RNA, Messenger / metabolism
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Rats
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Recombinant Proteins / drug effects
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Recombinant Proteins / metabolism
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Tetraethylammonium
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Tetraethylammonium Compounds / pharmacology
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Xenopus laevis
Substances
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Endothelins
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Phosphatidylinositols
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Potassium Channels
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RNA, Messenger
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Recombinant Proteins
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Tetraethylammonium Compounds
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Tetraethylammonium
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DNA