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/10.1152/ajpheart.00011.2012" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00011.2012</a>
Pages
H216–223
Issue
2
Volume
303
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
Disruption of TRPV1-mediated coupling of coronary blood flow to cardiac metabolism in diabetic mice: role of nitric oxide and BK channels.
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
2012
2012-07
Subject
The topic of the resource
13-dienoic Acid/pharmacology; 15-Hydroxy-11 alpha; 9 alpha-(epoxymethano)prosta-5; Anilides/pharmacology; Animals; Capsaicin/analogs & derivatives/pharmacology; Cinnamates/pharmacology; Coronary Vessels/drug effects/*metabolism/physiopathology; Diabetes Mellitus; Diabetic Cardiomyopathies/drug therapy/*metabolism; Enzyme Inhibitors/pharmacology; Inbred C57BL; Large-Conductance Calcium-Activated Potassium Channels/antagonists & inhibitors/*metabolism; Male; Mice; Microvessels/drug effects/physiopathology; NG-Nitroarginine Methyl Ester/pharmacology; Nitric Oxide/*metabolism; Peptides/pharmacology; TRPV Cation Channels/agonists/antagonists & inhibitors/biosynthesis/*metabolism; Type 2/drug therapy/*metabolism; Vasoconstrictor Agents/pharmacology; Vasodilation/drug effects
Creator
An entity primarily responsible for making the resource
Guarini Giacinta; Ohanyan Vahagn A; Kmetz John G; DelloStritto Daniel J; Thoppil Roslin J; Thodeti Charles K; Meszaros J Gary; Damron Derek S; Bratz Ian N
Description
An account of the resource
We have previously shown transient receptor potential vanilloid subtype 1 (TRPV1) channel-dependent coronary function is compromised in pigs with metabolic syndrome (MetS). However, the mechanisms through which TRPV1 channels couple coronary blood flow to metabolism are not fully understood. We employed mice lacking TRPV1 [TRPV1((-/-))], db/db diabetic, and control C57BKS/J mice to determine the extent to which TRPV1 channels modulate coronary function and contribute to vascular dysfunction in diabetic cardiomyopathy. Animals were subjected to in vivo infusion of the TRPV1 agonist capsaicin to examine the hemodynamic actions of TRPV1 activation. Capsaicin (1-100 mug.kg(-1).min(-1)) dose dependently increased coronary blood flow in control mice, which was inhibited by the TRPV1 antagonist capsazepine or the nitric oxide synthase (NOS) inhibitor N-nitro-l-arginine methyl ester (L-NAME). In addition, the capsaicin-mediated increase in blood flow was attenuated in db/db mice. TRPV1((-/-)) mice exhibited no changes in coronary blood flow in response to capsaicin. Vasoreactivity studies in isolated pressurized mouse coronary microvessels revealed a capsaicin-dependent relaxation that was inhibited by the TRPV1 inhibitor SB366791 l-NAME and to the large conductance calcium-sensitive potassium channel (BK) inhibitors iberiotoxin and Penetrim A. Similar to in vivo responses, capsaicin-mediated relaxation was impaired in db/db mice compared with controls. Changes in pH (pH 7.4-6.0) relaxed coronary vessels contracted to the thromboxane mimetic U46619 in all three groups of mice; however, pH-mediated relaxation was blunted in vessels obtained from TRPV1((-/-)) and db/db mice compared with controls. Western blot analysis revealed decreased myocardial TRPV1 protein expression in db/db mice compared with controls. Our data reveal TRPV1 channels mediate coupling of myocardial blood flow to cardiac metabolism via a nitric oxide-dependent, BK channel-dependent pathway that is corrupted in diabetes.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00011.2012" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00011.2012</a>
Rights
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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).
13-dienoic Acid/pharmacology
15-Hydroxy-11 alpha
2012
9 alpha-(epoxymethano)prosta-5
American journal of physiology. Heart and circulatory physiology
Anilides/pharmacology
Animals
Bratz Ian N
Capsaicin/analogs & derivatives/pharmacology
Cinnamates/pharmacology
Coronary Vessels/drug effects/*metabolism/physiopathology
Damron Derek S
DelloStritto Daniel J
Department of Integrative Medical Sciences
Diabetes Mellitus
Diabetic Cardiomyopathies/drug therapy/*metabolism
Enzyme Inhibitors/pharmacology
Guarini Giacinta
Inbred C57BL
Kmetz John G
Large-Conductance Calcium-Activated Potassium Channels/antagonists & inhibitors/*metabolism
Male
Meszaros J Gary
Mice
Microvessels/drug effects/physiopathology
NEOMED College of Medicine
NG-Nitroarginine Methyl Ester/pharmacology
Nitric Oxide/*metabolism
Ohanyan Vahagn A
Peptides/pharmacology
Thodeti Charles K
Thoppil Roslin J
TRPV Cation Channels/agonists/antagonists & inhibitors/biosynthesis/*metabolism
Type 2/drug therapy/*metabolism
Vasoconstrictor Agents/pharmacology
Vasodilation/drug effects
-
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/10.1016/j.yjmcc.2015.09.001" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.yjmcc.2015.09.001</a>
Pages
14–28
Volume
88
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
Overexpressing superoxide dismutase 2 induces a supernormal cardiac function by enhancing redox-dependent mitochondrial function and metabolic dilation.
Publisher
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Journal of molecular and cellular cardiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015-11
Subject
The topic of the resource
Adenosine Triphosphate/biosynthesis; Animals; Arterial Pressure/drug effects; Bioenergetics; Blood Flow Velocity/drug effects; Cardiac function; Cardiac/drug effects/*enzymology; Catalase/pharmacology; Echocardiography; Female; Gene Expression; Heart/drug effects/*enzymology; Hydrogen Peroxide/*metabolism/pharmacology; Injections; Intravenous; Male; Metabolic dilation; Mice; Mitochondria; Myocardium/*enzymology; Myocytes; NG-Nitroarginine Methyl Ester/pharmacology; Oxidation-Reduction; Oxygen Consumption/drug effects; Redox regulation; Signal Transduction; Stroke Volume/drug effects; Superoxide dismutase 2 (SOD2); Superoxide Dismutase/*genetics/metabolism; Transgenic; Transgenic mice; Vasodilation/*drug effects
Creator
An entity primarily responsible for making the resource
Kang Patrick T; Chen Chwen-Lih; Ohanyan Vahagn; Luther Daniel J; Meszaros J Gary; Chilian William M; Chen Yeong-Renn
Description
An account of the resource
During heightened cardiac work, O2 consumption by the heart benefits energy production via mitochondria. However, some electrons leak from the respiratory chain and yield superoxide, which is rapidly metabolized into H2O2 by SOD2. To understand the systemic effects of the metabolic dilator, H2O2, we studied mice with cardiac-specific SOD2 overexpression (SOD2-tg), which increases the H2O2 produced by cardiac mitochondria. Contrast echocardiography was employed to evaluate cardiac function, indicating that SOD2-tg had a significantly greater ejection fraction and a lower mean arterial pressure (MAP) that was partially normalized by intravenous injection of catalase. Norepinephrine-mediated myocardial blood flow (MBF) was significantly enhanced in SOD2-tg mice. Coupling of MBF to the double product (Heart RatexMAP) was increased in SOD2-tg mice, indicating that the metabolic dilator, "spilled" over, inducing systemic vasodilation. The hypothesis that SOD2 overexpression effectively enhances mitochondrial function was further evaluated. Mitochondria of SOD2-tg mice had a decreased state 3 oxygen consumption rate, but maintained the same ATP production flux under the basal and L-NAME treatment conditions, indicating a higher bioenergetic efficiency. SOD2-tg mitochondria produced less superoxide, and had lower redox activity in converting cyclic hydroxylamine to stable nitroxide, and a lower GSSG concentration. EPR analysis of the isolated mitochondria showed a significant decrease in semiquinones at the SOD2-tg Qi site. These results support a more reductive physiological setting in the SOD2-tg murine heart. Cardiac mitochondria exhibited no significant differences in the respiratory control index between WT and SOD2-tg. We conclude that SOD2 overexpression in myocytes enhances mitochondrial function and metabolic vasodilation, leading to a phenotype of supernormal cardiac function.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.yjmcc.2015.09.001" target="_blank" rel="noreferrer noopener">10.1016/j.yjmcc.2015.09.001</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).
2015
Adenosine Triphosphate/biosynthesis
Animals
Arterial Pressure/drug effects
Bioenergetics
Blood Flow Velocity/drug effects
Cardiac function
Cardiac/drug effects/*enzymology
Catalase/pharmacology
Chen Chwen-Lih
Chen Yeong-Renn
Chilian William M
Department of Integrative Medical Sciences
Echocardiography
Female
Gene Expression
Heart/drug effects/*enzymology
Hydrogen Peroxide/*metabolism/pharmacology
Injections
Intravenous
Journal of molecular and cellular cardiology
Kang Patrick T
Luther Daniel J
Male
Meszaros J Gary
Metabolic dilation
Mice
Mitochondria
Myocardium/*enzymology
Myocytes
NEOMED College of Medicine
NG-Nitroarginine Methyl Ester/pharmacology
Ohanyan Vahagn
Oxidation-Reduction
Oxygen Consumption/drug effects
Redox regulation
Signal Transduction
Stroke Volume/drug effects
Superoxide dismutase 2 (SOD2)
Superoxide Dismutase/*genetics/metabolism
Transgenic
Transgenic mice
Vasodilation/*drug effects