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<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
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Title
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Requisite Role of Kv1.5 Channels in Coronary Metabolic Dilation.
Publisher
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Circulation research
Date
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2015
2015-09
Subject
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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
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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
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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.
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<a href="http://doi.org/10.1161/CIRCRESAHA.115.306642" target="_blank" rel="noreferrer noopener">10.1161/CIRCRESAHA.115.306642</a>
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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