1
40
5
-
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>
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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/10.1161/ATVBAHA.113.301591" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/ATVBAHA.113.301591</a>
Pages
1911–1919
Issue
8
Volume
33
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
Mitochondrial oxidative stress corrupts coronary collateral growth by activating adenosine monophosphate activated kinase-alpha signaling.
Publisher
An entity responsible for making the resource available
Arteriosclerosis, thrombosis, and vascular biology
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013-08
Subject
The topic of the resource
AMP-Activated Protein Kinases/*metabolism; Animal; Animals; Body Weight/physiology; Cells; collateral circulation; coronary circulation; Coronary Vessels/cytology/*enzymology; Cultured; Disease Models; Endothelial Cells/cytology/*enzymology; Humans; Inbred WKY; Ischemia/metabolism/pathology; mitochondria; Mitochondria/drug effects/*metabolism; Myocardium/enzymology/pathology; Oxidative Stress/*physiology; Rats; reactive oxygen species; Rotenone/pharmacology; Signal Transduction/*physiology; TOR Serine-Threonine Kinases/metabolism; Uncoupling Agents/pharmacology
Creator
An entity primarily responsible for making the resource
Pung Yuh Fen; Sam Wai Johnn; Stevanov Kelly; Enrick Molly; Chen Chwen-Lih; Kolz Christopher; Thakker Prashanth; Hardwick James P; Chen Yeong-Renn; Dyck Jason R B; Yin Liya; Chilian William M
Description
An account of the resource
OBJECTIVE: Our goal was to determine the mechanism by which mitochondrial oxidative stress impairs collateral growth in the heart. APPROACH AND RESULTS: Rats were treated with rotenone (mitochondrial complex I inhibitor that increases reactive oxygen species production) or sham-treated with vehicle and subjected to repetitive ischemia protocol for 10 days to induce coronary collateral growth. In control rats, repetitive ischemia increased flow to the collateral-dependent zone; however, rotenone treatment prevented this increase suggesting that mitochondrial oxidative stress compromises coronary collateral growth. In addition, rotenone also attenuated mitochondrial complex I activity and led to excessive mitochondrial aggregation. To further understand the mechanistic pathway(s) involved, human coronary artery endothelial cells were treated with 50 ng/mL vascular endothelial growth factor, 1 micromol/L rotenone, and rotenone/vascular endothelial growth factor for 48 hours. Vascular endothelial growth factor induced robust tube formation; however, rotenone completely inhibited this effect (P\textless0.05 rotenone versus vascular endothelial growth factor treatment). Inhibition of tube formation by rotenone was also associated with significant increase in mitochondrial superoxide generation. Immunoblot analyses of human coronary artery endothelial cells with rotenone treatment showed significant activation of adenosine monophosphate activated kinase (AMPK)-alpha and inhibition of mammalian target of rapamycin and p70 ribosomal S6 kinase. Activation of AMPK-alpha suggested impairments in energy production, which was reflected by decrease in O2 consumption and bioenergetic reserve capacity of cultured cells. Knockdown of AMPK-alpha (siRNA) also preserved tube formation during rotenone, suggesting the negative effects were mediated by the activation of AMPK-alpha. Conversely, expression of a constitutively active AMPK-alpha blocked tube formation. CONCLUSIONS: We conclude that activation of AMPK-alpha during mitochondrial oxidative stress inhibits mammalian target of rapamycin signaling, which impairs phenotypic switching necessary for the growth of blood vessels.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/ATVBAHA.113.301591" target="_blank" rel="noreferrer noopener">10.1161/ATVBAHA.113.301591</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).
2013
AMP-Activated Protein Kinases/*metabolism
Animal
Animals
Arteriosclerosis, thrombosis, and vascular biology
Body Weight/physiology
Cells
Chen Chwen-Lih
Chen Yeong-Renn
Chilian William M
Collateral Circulation
Coronary Circulation
Coronary Vessels/cytology/*enzymology
Cultured
Department of Integrative Medical Sciences
Disease Models
Dyck Jason R B
Endothelial Cells/cytology/*enzymology
Enrick Molly
Hardwick James P
Humans
Inbred WKY
Ischemia/metabolism/pathology
Kolz Christopher
Mitochondria
Mitochondria/drug effects/*metabolism
Myocardium/enzymology/pathology
NEOMED College of Medicine
Oxidative Stress/*physiology
Pung Yuh Fen
Rats
reactive oxygen species
Rotenone/pharmacology
Sam Wai Johnn
Signal Transduction/*physiology
Stevanov Kelly
Thakker Prashanth
TOR Serine-Threonine Kinases/metabolism
Uncoupling Agents/pharmacology
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/10.1161/ATVBAHA.107.154294" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/ATVBAHA.107.154294</a>
Pages
61–67
Issue
1
Volume
28
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
The mechanistic basis for the disparate effects of angiotensin II on coronary collateral growth.
Publisher
An entity responsible for making the resource available
Arteriosclerosis, thrombosis, and vascular biology
Date
A point or period of time associated with an event in the lifecycle of the resource
2008
2008-01
Subject
The topic of the resource
Angiotensin; Angiotensin II/*physiology; Animal; Animals; Coronary Occlusion/drug therapy/*physiopathology; Disease Models; Hemorheology; Ischemia/drug therapy/*physiopathology; Male; Neovascularization; Oxidative Stress/*physiology; Physiologic/*physiology; Rats; Reactive Oxygen Species/adverse effects/metabolism; Receptor; Type 1/*drug effects/physiology; Vasoconstrictor Agents/pharmacology
Creator
An entity primarily responsible for making the resource
Reed Ryan; Kolz Christopher; Potter Barry; Rocic Petra
Description
An account of the resource
OBJECTIVE: We hypothesize that controversial effects of angiotensin II (Ang II) are attributable to its regulation of reactive oxygen species (ROS) and
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/ATVBAHA.107.154294" target="_blank" rel="noreferrer noopener">10.1161/ATVBAHA.107.154294</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).
2008
Angiotensin
Angiotensin II/*physiology
Animal
Animals
Arteriosclerosis, thrombosis, and vascular biology
Coronary Occlusion/drug therapy/*physiopathology
Disease Models
Hemorheology
Ischemia/drug therapy/*physiopathology
Kolz Christopher
Male
Neovascularization
Oxidative Stress/*physiology
Physiologic/*physiology
Potter Barry
Rats
Reactive Oxygen Species/adverse effects/metabolism
Receptor
Reed Ryan
Rocic Petra
Type 1/*drug effects/physiology
Vasoconstrictor Agents/pharmacology
-
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/10.1152/ajpheart.01330.2006" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.01330.2006</a>
Pages
H2729–2736
Issue
6
Volume
292
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
Optimal reactive oxygen species concentration and p38 MAP kinase are required for coronary collateral growth.
Publisher
An entity responsible for making the resource available
American journal of physiology. Heart and circulatory physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2007
2007-06
Subject
The topic of the resource
*Collateral Circulation/drug effects; *Coronary Circulation/drug effects; *MAP Kinase Signaling System/drug effects; Acetophenones/pharmacology; Animal; Animals; Blood Flow Velocity; Cells; Coronary Vessels/surgery; Cultured; Disease Models; Ditiocarb/pharmacology; Endothelial Cells/drug effects/enzymology/*metabolism; Enzyme Inhibitors/pharmacology; Humans; Imidazoles/pharmacology; Inbred WKY; Ligation; Male; Myocardial Reperfusion Injury/enzymology/metabolism/*physiopathology; NADPH Oxidases/antagonists & inhibitors/metabolism; Neovascularization; Onium Compounds/pharmacology; Oxygenases/antagonists & inhibitors/metabolism; p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors/*metabolism; Physiologic; Pyridines/pharmacology; Rats; Reactive Oxygen Species/*metabolism; Superoxide Dismutase/antagonists & inhibitors/metabolism; Vascular Endothelial Growth Factor A/metabolism
Creator
An entity primarily responsible for making the resource
Rocic Petra; Kolz Christopher; Reed Ryan; Potter Barry; Chilian William M
Description
An account of the resource
Reactive oxygen species (ROS) are implicated in coronary collateral growth (CCG). We evaluated the requirement for ROS in human coronary artery endothelial cell (HCAEC) tube formation, CCG in vivo, and signaling (p38 MAP kinase) by which ROS may stimulate vascular growth. The flavin-containing oxidase inhibitor diphenyleneiodonium (DPI) or the superoxide dismutase inhibitor diethyldithiocarbamate (DETC) blocked vascular endothelial growth factor-induced HCAEC tube formation in Matrigel. We assessed the effect of DPI and DETC on CCG in a rat model of repetitive ischemia (RI) (40 s left anterior descending coronary artery occlusion every 20 min for 2 h 20 min, 3 times/day, 10 days). DPI or DETC was given intraperitoneally, or the NAD(P)H oxidase inhibitor apocynin was given in drinking water. Collateral-dependent flow (measured by using microspheres) was expressed as a ratio of normal and ischemic zone flows. In sham-operated rats, collateral flow in the ischemic zone was 18 +/- 6% of normal zone; in the RI group, collateral flow in the ischemic zone was 83 +/- 5% of normal zone. DPI prevented the increase in collateral flow after RI (25 +/- 4% of normal zone). Similar results were obtained with apocynin following RI (32 +/- 7% of that in the normal zone). DETC achieved similar results (collateral flow after RI was 21 +/- 2% of normal zone). DPI and DETC blocked RI-induced p38 MAP kinase activation in response to vascular endothelial growth factor and RI. These results demonstrate a requirement for optimal ROS concentration in HCAEC tube formation, CCG, and p38 MAP kinase activation. p38 MAP kinase inhibition prevented HCAEC tube formation and partially blocked RI-induced CCG (42 +/- 7% of normal zone flow), indicating that p38 MAP kinase is a critical signaling mediator of CCG.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.01330.2006" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.01330.2006</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).
*Collateral Circulation/drug effects
*Coronary Circulation/drug effects
*MAP Kinase Signaling System/drug effects
2007
Acetophenones/pharmacology
American journal of physiology. Heart and circulatory physiology
Animal
Animals
Blood Flow Velocity
Cells
Chilian William M
Coronary Vessels/surgery
Cultured
Department of Integrative Medical Sciences
Disease Models
Ditiocarb/pharmacology
Endothelial Cells/drug effects/enzymology/*metabolism
Enzyme Inhibitors/pharmacology
Humans
Imidazoles/pharmacology
Inbred WKY
Kolz Christopher
Ligation
Male
Myocardial Reperfusion Injury/enzymology/metabolism/*physiopathology
NADPH Oxidases/antagonists & inhibitors/metabolism
NEOMED College of Medicine
Neovascularization
Onium Compounds/pharmacology
Oxygenases/antagonists & inhibitors/metabolism
p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors/*metabolism
Physiologic
Potter Barry
Pyridines/pharmacology
Rats
Reactive Oxygen Species/*metabolism
Reed Ryan
Rocic Petra
Superoxide Dismutase/antagonists & inhibitors/metabolism
Vascular Endothelial Growth Factor A/metabolism
-
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