Cloning and modulation by endothelin-1 of rat cardiac K channel

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 (I RH1) was studied using Xeno...

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Veröffentlicht in:	Biochemical and biophysical research communications 1992-05, Vol.184 (3), p.1484-1489
Hauptverfasser:	Ishii, Kuniaki, Nunoki, Kazuo, Murakoshi, Hideyuki, Taira, Norio
Format:	Artikel
Sprache:	eng
Schlagworte:	amino acid sequence Animals association Biological and medical sciences cDNA Cell physiology Cloning, Molecular DNA - genetics endothelin-1 receptors Endothelins - pharmacology Evoked Potentials - drug effects Female Fundamental and applied biological sciences. Psychology genes Genetic Vectors heart Heart - physiology Male Membrane and intracellular transports Membrane Potentials - drug effects Molecular and cellular biology nucleotide sequence Oocytes - drug effects Oocytes - physiology Phosphatidylinositols - metabolism potassium channels Potassium Channels - drug effects Potassium Channels - genetics Potassium Channels - physiology predictions Rats Recombinant Proteins - drug effects Recombinant Proteins - metabolism RNA, Messenger - genetics RNA, Messenger - metabolism Tetraethylammonium Tetraethylammonium Compounds - pharmacology Xenopus laevis
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Beschreibung
Zusammenfassung:	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 (I RH1) was studied using Xenopus oocyte expression system. Activation of two different subtypes of ETRs by endothelin-1 equally suppressed the amplitude of I RH1. Stimulation of phosphatidylinositol turnover will probably be responsible for the suppression.
ISSN:	0006-291X 1090-2104
DOI:	10.1016/S0006-291X(05)80050-6