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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.1997.273.6.h2613" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.1997.273.6.h2613</a>
Pages
H2613–2619
Issue
6
Volume
273
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
Daily exercise attenuates the sympathetic component of the arterial baroreflex control of heart rate.
Publisher
An entity responsible for making the resource available
The American journal of physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
1997
1997-12
Subject
The topic of the resource
Animal/*physiology; Animals; Arteries/drug effects/innervation/*physiology; Baroreflex/drug effects/*physiology; Body Weight; Female; Heart Rate/*physiology; Heart/anatomy & histology/*physiology; Nitroprusside/pharmacology; Organ Size; Parasympathetic Nervous System/physiology; Phenylephrine/pharmacology; Physical Conditioning; Pulse; Rats; Sympathetic Nervous System/physiology
Creator
An entity primarily responsible for making the resource
Collins H L; DiCarlo S E
Description
An account of the resource
The influence of daily spontaneous running (DSR) on the sympathetic (SC) and parasympathetic components of the arterial baroreflex control of heart rate (HR) was examined in 16 female Long Evans rats [8 sedentary (SED) and 8 DSR]. After
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.1997.273.6.h2613" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.1997.273.6.h2613</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).
1997
Animal/*physiology
Animals
Arteries/drug effects/innervation/*physiology
Baroreflex/drug effects/*physiology
Body Weight
Collins H L
DiCarlo S E
Female
Heart Rate/*physiology
Heart/anatomy & histology/*physiology
Nitroprusside/pharmacology
Organ Size
Parasympathetic Nervous System/physiology
Phenylephrine/pharmacology
Physical Conditioning
Pulse
Rats
Sympathetic Nervous System/physiology
The American journal of physiology
-
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.00436.2007" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00436.2007</a>
Pages
H3720–3725
Issue
6
Volume
293
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
Redox-dependent coronary metabolic dilation.
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
2007-12
Subject
The topic of the resource
*Paracrine Communication; *Vasodilation/drug effects; Acetylcysteine/pharmacology; Animals; Antioxidants/pharmacology; Cardiac/drug effects/*metabolism; Conditioned/metabolism; Coronary Vessels/drug effects/enzymology/*metabolism; Culture Media; Dithiothreitol/pharmacology; Enzyme Activation; Fluorescence; Hydrogen Peroxide/metabolism; Imidazoles/pharmacology; In Vitro Techniques; Microscopy; Myocytes; Nitroprusside/pharmacology; Oxidation-Reduction; p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors/metabolism; Phosphorylation; Protein Kinase Inhibitors/pharmacology; Pyridines/pharmacology; Rats; Reactive Oxygen Species/*metabolism; Reducing Agents/pharmacology; Sulfhydryl Compounds/*metabolism; Vasodilator Agents/pharmacology; Wistar
Creator
An entity primarily responsible for making the resource
Saitoh Shu-ichi; Kiyooka Takahiko; Rocic Petra; Rogers Paul A; Zhang Cuihua; Swafford Albert; Dick Gregory M; Viswanathan Chandrasekar; Park Yoonjung; Chilian William M
Description
An account of the resource
We have observed that hydrogen peroxide (H2O2), the dismutated product of superoxide, is a coronary metabolic dilator and couples myocardial oxygen consumption to coronary blood flow. Because the chemical activity of H2O2 favors its role as an oxidant, and thiol groups are susceptible to oxidation, we hypothesized that coronary metabolic dilation occurs via a redox mechanism involving thiol oxidation. To test this hypothesis, we studied the mechanisms of dilation of isolated coronary arterioles to metabolites released by metabolically active (paced at 400 min) isolated cardiac myocytes and directly compared these responses with authentic H2O2. Studies were performed under control conditions and using interventions designed to reduce oxidized thiols [0.1 microM dithiothreitol (DTT) and 10 mM N-acetyl-L-cysteine (NAC)]. Aliquots of the conditioned buffer from paced myocytes produced vasodilation of isolated arterioles (peak response, 71% +/- 6% of maximal dilation), whereas H2O2 produced complete dilation (92% +/- 7%). Dilation to either the conditioned buffer or to H2O2 was significantly reduced by the administration of either NAC or DTT. The location of the thiols oxidized by the conditioned buffer or of H2O2 was determined by the administration of the fluorochromes monochlorobimane (20 microM) or monobromotrimethylammoniobimane (20 microM), which covalently label the reduced total or extracellular-reduced thiols, respectively. H2O2 or the conditioned buffer predominantly oxidized intracellular thiols since the fluorescent signal from monochlorobimane was reduced more than that of monobromotrimethylammoniobimane. To determine whether one of the intracellular targets of thiol oxidation that leads to dilation is the redox-sensitive kinase p38 mitogen-activated protein (MAP) kinase, we evaluated dilation following the administration of the p38 inhibitor SB-203580 (10 microM). The inhibition of p38 attenuated dilation to either H2O2 or to the conditioned buffer from stimulated myocytes by a similar degree, but SB-203580 did not attenuate dilation to nitroprusside. Western blot analysis for the activated form of p38 (phospho-p38) in the isolated aortae revealed robust activation of this enzyme by H2O2. Taken together, our results show that an active component of cardiac metabolic dilation, like that of H2O2, produces dilation by the oxidation of thiols, which are predominantly intracellular and dependent activation on the p38 MAP kinase. Thus coronary metabolic dilation appears to be mediated by redox-dependent signals.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00436.2007" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00436.2007</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).
*Paracrine Communication
*Vasodilation/drug effects
2007
Acetylcysteine/pharmacology
American journal of physiology. Heart and circulatory physiology
Animals
Antioxidants/pharmacology
Cardiac/drug effects/*metabolism
Chilian William M
Conditioned/metabolism
Coronary Vessels/drug effects/enzymology/*metabolism
Culture Media
Department of Integrative Medical Sciences
Dick Gregory M
Dithiothreitol/pharmacology
Enzyme Activation
Fluorescence
Hydrogen Peroxide/metabolism
Imidazoles/pharmacology
In Vitro Techniques
Kiyooka Takahiko
Microscopy
Myocytes
NEOMED College of Medicine
Nitroprusside/pharmacology
Oxidation-Reduction
p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors/metabolism
Park Yoonjung
Phosphorylation
Protein Kinase Inhibitors/pharmacology
Pyridines/pharmacology
Rats
Reactive Oxygen Species/*metabolism
Reducing Agents/pharmacology
Rocic Petra
Rogers Paul A
Saitoh Shu-ichi
Sulfhydryl Compounds/*metabolism
Swafford Albert
Vasodilator Agents/pharmacology
Viswanathan Chandrasekar
Wistar
Zhang Cuihua