1
40
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Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1161/CIRCRESAHA.115.306642" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/CIRCRESAHA.115.306642</a>
Pages
612–621
Issue
7
Volume
117
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Requisite Role of Kv1.5 Channels in Coronary Metabolic Dilation.
Publisher
An entity responsible for making the resource available
Circulation research
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015-09
Subject
The topic of the resource
129 Strain; Animals; cardiac function; contrast echocardiography; Coronary Circulation/*physiology; Coronary Vessels/*metabolism; hydrogen peroxide; Inbred C57BL; ion channel; Knockout; Kv1.5 Potassium Channel/*physiology; Mice; Muscle; Smooth; Transgenic; transgenic mice; Vascular/*metabolism; vasodilation; Vasodilation/*physiology; voltage-gated potassium channels
Creator
An entity primarily responsible for making the resource
Ohanyan Vahagn; Yin Liya; Bardakjian Raffi; Kolz Christopher; Enrick Molly; Hakobyan Tatevik; Kmetz John; Bratz Ian; Luli Jordan; Nagane Masaki; Khan Nadeem; Hou Huagang; Kuppusamy Periannan; Graham Jacqueline; Fu Frances Kwan; Janota Danielle; Oyewumi Moses O; Logan Suzanna; Lindner Jonathan R; Chilian William M
Description
An account of the resource
RATIONALE: In the working heart, coronary blood flow is linked to the production of metabolites, which modulate tone of smooth muscle in a redox-dependent manner. Voltage-gated potassium channels (Kv), which play a role in controlling membrane potential in vascular smooth muscle, have certain members that are redox-sensitive. OBJECTIVE: To determine the role of redox-sensitive Kv1.5 channels in coronary metabolic flow regulation. METHODS AND RESULTS: In mice (wild-type [WT], Kv1.5 null [Kv1.5(-/-)], and Kv1.5(-/-) and WT with inducible, smooth muscle-specific expression of Kv1.5 channels), we measured mean arterial pressure, myocardial blood flow, myocardial tissue oxygen tension, and ejection fraction before and after inducing cardiac stress with norepinephrine. Cardiac work was estimated as the product of mean arterial pressure and heart rate. Isolated arteries were studied to establish whether genetic alterations modified vascular reactivity. Despite higher levels of cardiac work in the Kv1.5(-/-) mice (versus WT mice at baseline and all doses of norepinephrine), myocardial blood flow was lower in Kv1.5(-/-) mice than in WT mice. At high levels of cardiac work, tissue oxygen tension dropped significantly along with ejection fraction. Expression of Kv1.5 channels in smooth muscle in the null background rescued this phenotype of impaired metabolic dilation. In isolated vessels from Kv1.5(-/-) mice, relaxation to H2O2 was impaired, but responses to adenosine and acetylcholine were normal compared with those from WT mice. CONCLUSIONS: Kv1.5 channels in vascular smooth muscle play a critical role in coupling myocardial blood flow to cardiac metabolism. Absence of these channels disassociates metabolism from flow, resulting in cardiac pump dysfunction and tissue hypoxia.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/CIRCRESAHA.115.306642" target="_blank" rel="noreferrer noopener">10.1161/CIRCRESAHA.115.306642</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
129 Strain
2015
Animals
Bardakjian Raffi
Bratz Ian
Cardiac function
Chilian William M
Circulation research
contrast echocardiography
Coronary Circulation/*physiology
Coronary Vessels/*metabolism
Department of Integrative Medical Sciences
Department of Pharmaceutical Sciences
Enrick Molly
Fu Frances Kwan
Graham Jacqueline
Hakobyan Tatevik
Hou Huagang
Hydrogen peroxide
Inbred C57BL
ion channel
Janota Danielle
Khan Nadeem
Kmetz John
Knockout
Kolz Christopher
Kuppusamy Periannan
Kv1.5 Potassium Channel/*physiology
Lindner Jonathan R
Logan Suzanna
Luli Jordan
Mice
Muscle
Nagane Masaki
NEOMED College of Medicine
NEOMED College of Pharmacy
Ohanyan Vahagn
Oyewumi Moses O
Smooth
Transgenic
Transgenic mice
Vascular/*metabolism
vasodilation
Vasodilation/*physiology
voltage-gated potassium channels
Yin Liya
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1111/micc.12334" target="_blank" rel="noreferrer noopener">http://doi.org/10.1111/micc.12334</a>
Issue
4
Volume
24
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Kv1.3 channels facilitate the connection between metabolism and blood flow in the heart.
Publisher
An entity responsible for making the resource available
Microcirculation (New York, N.Y. : 1994)
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-05
Subject
The topic of the resource
*contrast echocardiography; *coronary blood flow; *Coronary Circulation/drug effects; *coronary microcirculation; *Kv 1.3 channels; Animals; Kv1.3 Potassium Channel/*physiology; Mice; Myocardium/*metabolism; Potassium Channel Blockers/pharmacology; Regional Blood Flow/drug effects; Triterpenes/pharmacology; Vasodilation/drug effects
Creator
An entity primarily responsible for making the resource
Ohanyan Vahagn; Yin Liya; Bardakjian Raffi; Kolz Christopher; Enrick Molly; Hakobyan Tatevik; Luli Jordan; Graham Kathleen; Khayata Mohamed; Logan Suzanna; Kmetz John; Chilian William M
Description
An account of the resource
The connection between metabolism and flow in the heart, metabolic dilation, is essential for cardiac function. We recently found redox-sensitive Kv1.5 channels play a role in coronary metabolic dilation; however, more than one ion channel likely plays a role in this process as animals null for these channels still showed limited coronary metabolic dilation. Accordingly, we examined the role of another Kv1 family channel, the energetically linked Kv1.3 channel, in coronary metabolic dilation. We measured myocardial blood flow (contrast echocardiography) during norepinephrine-induced increases in cardiac work (heart rate x mean arterial pressure) in WT, WT mice given correolide (preferential Kv1.3 antagonist), and Kv1.3-null mice (Kv1.3(-/-) ). We also measured relaxation of isolated small arteries mounted in a myograph. During increased cardiac work, myocardial blood flow was attenuated in Kv1.3(-/-) and in correolide-treated mice. In isolated vessels from Kv1.3(-/-) mice, relaxation to H2 O2 was impaired (vs WT), but responses to adenosine and acetylcholine were equivalent to WT. Correolide reduced dilation to adenosine and acetylcholine in WT and Kv1.3(-/-) , but had no effect on H2 O2 -dependent dilation in vessels from Kv1.3(-/-) mice. We conclude that Kv1.3 channels participate in the connection between myocardial blood flow and cardiac metabolism.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1111/micc.12334" target="_blank" rel="noreferrer noopener">10.1111/micc.12334</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*contrast echocardiography
*coronary blood flow
*Coronary Circulation/drug effects
*coronary microcirculation
*Kv 1.3 channels
2017
Animals
Bardakjian Raffi
Chilian William M
Department of Integrative Medical Sciences
Enrick Molly
Graham Kathleen
Hakobyan Tatevik
Khayata Mohamed
Kmetz John
Kolz Christopher
Kv1.3 Potassium Channel/*physiology
Logan Suzanna
Luli Jordan
Mice
Microcirculation (New York, N.Y. : 1994)
Myocardium/*metabolism
NEOMED College of Medicine
Ohanyan Vahagn
Potassium Channel Blockers/pharmacology
Regional Blood Flow/drug effects
Triterpenes/pharmacology
Vasodilation/drug effects
Yin Liya