| TWIK-related two-pore domain potassium channel TREK-1 in carotid endothelium of normotensive and hypertensive mice. | |
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MedLine Citation:
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PMID: 18339646 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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AIMS: Potassium channels are essential elements of endothelial function. Recently, evidence emerged that the TWIK (tandem of P domains in a weak inwardly rectifying K+ channel)-related K+ channel (TREK-1) of the two-pore domain potassium channel gene family (K2P) may be involved in the regulation of vascular tone. However, the functional and molecular characterization of vascular TREK-1 is incomplete. In this study, we therefore analysed the functional expression of TREK-1 in the endothelium. Moreover, we hypothesized that changes in channel expression may contribute to altered endothelial vasodilator response under conditions of elevated blood pressure. METHODS AND RESULTS: Gene expression and function of endothelial TREK-1 were analysed by single-cell RT-PCR, the patch-clamp technique and pressure myography in murine carotid arteries (CA). K+ outward currents displaying the characteristics of TREK-1 were observed following various TREK-1-activating stimuli such as membrane stretch, intracellular acidosis, polyunsaturated fatty acids, isoflurane (ISOFL), riluzole, and acetylcholine (ACh). In K(Ca)3.1(-/-) mice exhibiting elevated blood pressure, endothelial TREK-1 currents and TREK-1 mRNA expression were enhanced as compared with normotensive control mice. TREK-1-mediated vasodilator responses to alpha-linolenic acid, ISOFL, or ACh were increased. A similar up-regulation of endothelial TREK-1 was observed in spontaneously hypertensive rats. CONCLUSION: We have found that TREK-1 is an endothelial K+ channel capable of producing hyperpolarization and vasodilation. A correlation between hypertension and up-regulation of TREK-1 was observed in two different animal models of elevated blood pressure. Thus, TREK-1 may play a protective role in the cardiovascular system by providing a novel type of endothelial hyperpolarization-mediated vasodilator response. |
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Authors:
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Sebastian Pokojski; Christoph Busch; Ivica Grgic; Michael Kacik; Waleed Salman; Regina Preisig-Müller; Willm-Thomas Heyken; Jürgen Daut; Joachim Hoyer; Ralf Köhler |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Retracted Publication Date: 2008-03-13 |
Journal Detail:
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Title: Cardiovascular research Volume: 79 ISSN: 0008-6363 ISO Abbreviation: Cardiovasc. Res. Publication Date: 2008 Jul |
Date Detail:
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Created Date: 2008-06-16 Completed Date: 2008-10-14 Revised Date: 2008-12-16 |
Medline Journal Info:
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Nlm Unique ID: 0077427 Medline TA: Cardiovasc Res Country: Netherlands |
Other Details:
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Languages: eng Pagination: 80-8 Citation Subset: IM |
Affiliation:
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Department of Internal Medicine-Nephrology, Philipps-University, Baldingerstrasse, 35033 Marburg, Hessen, Germany. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Blood Pressure / physiology Carotid Arteries / cytology, metabolism*, pathology Disease Models, Animal Endothelium, Vascular / cytology, metabolism*, pathology Hypertension / metabolism*, pathology, physiopathology Male Mice Mice, Knockout Patch-Clamp Techniques Potassium Channels, Tandem Pore Domain / genetics, metabolism* Protein Structure, Tertiary / genetics Rats Rats, Inbred SHR Rats, Inbred WKY Up-Regulation / physiology Vasodilation / physiology |
| Chemical | |
Reg. No./Substance:
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0/Kcnk1 protein, mouse; 0/Kcnk1 protein, rat; 0/Potassium Channels, Tandem Pore Domain; 0/potassium channel protein TREK-1 |
| Comments/Corrections | |
Retraction In:
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Pokojski S, Busch C, Grgic I, Kacik M, Salman W, Preisig-Müller R, Heyken WT, Daut J, Hoyer J, Köhler R. Cardiovasc Res. 2008 Nov 1;80(2):320
[PMID:
18922814
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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