1
40
11
-
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.00142.2011" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00142.2011</a>
Pages
H757–765
Issue
3
Volume
301
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
PKCalpha mediates acetylcholine-induced activation of TRPV4-dependent calcium influx in endothelial cells.
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
2011
2011-09
Subject
The topic of the resource
Acetylcholine/*pharmacology; Animals; Calcium Signaling/*drug effects; Carbazoles/pharmacology; Cells; Cultured; Endothelial Cells/*drug effects/enzymology; Enzyme Activation; Inbred C57BL; Knockout; Male; Mesenteric Arteries/drug effects/enzymology; Mice; Mutation; Nitric Oxide Synthase Type III/metabolism; Phosphorylation; Protein Kinase C-alpha/genetics/*metabolism; Protein Kinase Inhibitors/pharmacology; Tetradecanoylphorbol Acetate/pharmacology; Time Factors; Transfection; TRPV Cation Channels/*agonists/deficiency/genetics/metabolism; Vasodilation/*drug effects; Vasodilator Agents/*pharmacology
Creator
An entity primarily responsible for making the resource
Adapala Ravi K; Talasila Phani K; Bratz Ian N; Zhang David X; Suzuki Makoto; Meszaros J Gary; Thodeti Charles K
Description
An account of the resource
Transient receptor potential vanilloid channel 4 (TRPV4) is a polymodally activated nonselective cationic channel implicated in the regulation of vasodilation and hypertension. We and others have recently shown that cyclic stretch and shear stress activate TRPV4-mediated calcium influx in endothelial cells (EC). In addition to the mechanical forces, acetylcholine (ACh) was shown to activate TRPV4-mediated calcium influx in endothelial cells, which is important for nitric oxide-dependent vasodilation. However, the molecular mechanism through which ACh activates TRPV4 is not known. Here, we show that ACh-induced calcium influx and endothelial nitric oxide synthase (eNOS) phosphorylation but not calcium release from intracellular stores is inhibited by a specific TRPV4 antagonist, AB-159908. Importantly, activation of store-operated calcium influx was not altered in the TRPV4 null EC, suggesting that
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00142.2011" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00142.2011</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).
2011
Acetylcholine/*pharmacology
Adapala Ravi K
American journal of physiology. Heart and circulatory physiology
Animals
Bratz Ian N
Calcium Signaling/*drug effects
Carbazoles/pharmacology
Cells
Cultured
Department of Integrative Medical Sciences
Endothelial Cells/*drug effects/enzymology
Enzyme Activation
Inbred C57BL
Knockout
Male
Mesenteric Arteries/drug effects/enzymology
Meszaros J Gary
Mice
Mutation
NEOMED College of Medicine
Nitric Oxide Synthase Type III/metabolism
Phosphorylation
Protein Kinase C-alpha/genetics/*metabolism
Protein Kinase Inhibitors/pharmacology
Suzuki Makoto
Talasila Phani K
Tetradecanoylphorbol Acetate/pharmacology
Thodeti Charles K
Time Factors
Transfection
TRPV Cation Channels/*agonists/deficiency/genetics/metabolism
Vasodilation/*drug effects
Vasodilator Agents/*pharmacology
Zhang David X
-
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/10.1080/19336950.2017.1365206" target="_blank" rel="noreferrer noopener">http://doi.org/10.1080/19336950.2017.1365206</a>
Pages
587–603
Issue
6
Volume
11
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
TRPA1 ion channel stimulation enhances cardiomyocyte contractile function via a CaMKII-dependent pathway.
Publisher
An entity responsible for making the resource available
Channels (Austin, Tex.)
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-11
Subject
The topic of the resource
[Ca2+]i; *Myocardial Contraction; Animals; Calcium-Calmodulin-Dependent Protein Kinase Type 2/*metabolism; CaMKII; Cardiac/*metabolism; cardiomyocytes; contractility; Inbred C57BL; Knockout; Mice; Myocytes; TRPA1; TRPA1 Cation Channel/deficiency/*metabolism
Creator
An entity primarily responsible for making the resource
Andrei Spencer R; Ghosh Monica; Sinharoy Pritam; Dey Souvik; Bratz Ian N; Damron Derek S
Description
An account of the resource
RATIONALE: Transient receptor potential channels of the ankyrin subtype-1 (TRPA1) are non-selective cation channels that show high permeability to calcium. Previous studies from our laboratory have demonstrated that TRPA1 ion channels are expressed in adult mouse ventricular cardiomyocytes (CMs) and are localized at the z-disk, costamere and intercalated disk. The functional significance of TRPA1 ion channels in the modulation of CM contractile function have not been explored. OBJECTIVE: To identify the extent to which TRPA1 ion channels are involved in modulating CM contractile function and elucidate the cellular mechanism of action. METHODS AND RESULTS: Freshly isolated CMs were obtained from murine heart and loaded with Fura-2 AM. Simultaneous measurement of intracellular free Ca(2+) concentration ([Ca(2+)]i) and contractility was performed in individual CMs paced at 0.3 Hz. Our findings demonstrate that TRPA1 stimulation with AITC results in a dose-dependent increase in peak [Ca(2+)]i and a concomitant increase in CM fractional shortening. Further analysis revealed a dose-dependent acceleration in time to peak [Ca(2+)]i and velocity of shortening as well as an acceleration in [Ca(2+)]i decay and velocity of relengthening. These effects of TRPA1 stimulation were not observed in CMs pre-treated with the TRPA1 antagonist, HC-030031 (10 micromol/L) nor in CMs obtained from TRPA1(-/-) mice. Moreover, we observed no significant increase in cAMP levels or PKA activity in response to TRPA1 stimulation and the PKA inhibitor peptide (PKI
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1080/19336950.2017.1365206" target="_blank" rel="noreferrer noopener">10.1080/19336950.2017.1365206</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).
[Ca2+]i
*Myocardial Contraction
2017
Andrei Spencer R
Animals
Bratz Ian N
Calcium-Calmodulin-Dependent Protein Kinase Type 2/*metabolism
CaMKII
Cardiac/*metabolism
cardiomyocytes
Channels (Austin, Tex.)
contractility
Damron Derek S
Dey Souvik
Ghosh Monica
Inbred C57BL
Knockout
Mice
Myocytes
Sinharoy Pritam
TRPA1
TRPA1 Cation Channel/deficiency/*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/10.1080/19336950.2016.1185579" target="_blank" rel="noreferrer noopener">http://doi.org/10.1080/19336950.2016.1185579</a>
Pages
395–409
Issue
5
Volume
10
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
TRPA1 is functionally co-expressed with TRPV1 in cardiac muscle: Co-localization at z-discs, costameres and intercalated discs.
Publisher
An entity responsible for making the resource available
Channels (Austin, Tex.)
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-09
Subject
The topic of the resource
Animals; Ca2+; Calcium/physiology; Cardiac/*physiology; cardiomyocytes; Inbred C57BL; Male; Mice; Myocytes; Transient Receptor Potential Channels/genetics/*physiology; TRPA1; TRPA1 Cation Channel; TRPV Cation Channels/genetics/*physiology; TRPV1; Z-disc
Creator
An entity primarily responsible for making the resource
Andrei Spencer R; Sinharoy Pritam; Bratz Ian N; Damron Derek S
Description
An account of the resource
Transient receptor potential channels of the ankyrin subtype-1 (TRPA1) and vanilloid subtype-1 (TRPV1) are structurally related, non-selective cation channels that show a high permeability to calcium. Previous studies indicate that TRP channels play a prominent role in the regulation of cardiovascular dynamics and homeostasis, but also contribute to the pathophysiology of many diseases and disorders within the cardiovascular system. However, no studies to date have identified the functional expression and/or intracellular localization of TRPA1 in primary adult mouse ventricular cardiomyocytes (CMs). Although TRPV1 has been implicated in the regulation of cardiac function, there is a paucity of information regarding functional expression and localization of TRPV1 in adult CMs. Our current studies demonstrate that TRPA1 and TRPV1 ion channels are co-expressed at the protein level in CMs and both channels are expressed throughout the endocardium, myocardium and epicardium. Moreover, immunocytochemical localization demonstrates that both channels predominantly colocalize at the Z-discs, costameres and intercalated discs. Furthermore, specific TRPA1 and TRPV1 agonists elicit dose-dependent, transient rises in intracellular free calcium concentration ([Ca(2+)]i) that are abolished in CMs obtained from TRPA1(-/-) and TRPV1(-/-) mice. Similarly, we observed a dose-dependent attenuation of the TRPA1 and TRPV1 agonist-induced increase in [Ca(2+)]i when WT CMs were pretreated with increasing concentrations of selective TRPA1 or TRPV1 channel antagonists. In summary, these findings demonstrate functional expression and the precise ultrastructural localization of TRPA1 and TRPV1 ion channels in freshly isolated mouse CMs. Crosstalk between TRPA1 and TRPV1 may be important in mediating cellular signaling events in cardiac muscle.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1080/19336950.2016.1185579" target="_blank" rel="noreferrer noopener">10.1080/19336950.2016.1185579</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).
2016
Andrei Spencer R
Animals
Bratz Ian N
Ca2+
Calcium/physiology
Cardiac/*physiology
cardiomyocytes
Channels (Austin, Tex.)
Damron Derek S
Inbred C57BL
Male
Mice
Myocytes
Sinharoy Pritam
Transient Receptor Potential Channels/genetics/*physiology
TRPA1
TRPA1 Cation Channel
TRPV Cation Channels/genetics/*physiology
TRPV1
Z-disc
-
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/10.1007/s00395-016-0539-4" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s00395-016-0539-4</a>
Pages
21–21
Issue
2
Volume
111
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
Differential regulation of TRPV1 channels by H2O2: implications for diabetic microvascular dysfunction.
Publisher
An entity responsible for making the resource available
Basic research in cardiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-03
Subject
The topic of the resource
*Coronary Circulation; *Microcirculation; Animals; Capsaicin; Coronary blood flow; Diabetic Angiopathies/*metabolism; HEK293 Cells; Humans; Hydrogen peroxide; Hydrogen Peroxide/*metabolism; Inbred C57BL; Knockout; Male; Mice; Reactive oxygen species; TRPV Cation Channels/*metabolism; TRPV1
Creator
An entity primarily responsible for making the resource
DelloStritto Daniel J; Connell Patrick J; Dick Gregory M; Fancher Ibra S; Klarich Brittany; Fahmy Joseph N; Kang Patrick T; Chen Yeong-Renn; Damron Derek S; Thodeti Charles K; Bratz Ian N
Description
An account of the resource
We demonstrated previously that TRPV1-dependent coupling of coronary blood flow (CBF) to metabolism is disrupted in diabetes. A critical amount of H2O2 contributes to CBF regulation; however, excessive H2O2 impairs responses. We sought to determine the extent to which differential regulation of TRPV1 by H2O2 modulates CBF and vascular reactivity in diabetes. We used contrast echocardiography to study TRPV1 knockout (V1KO), db/db diabetic, and wild type C57BKS/J (WT) mice. H2O2 dose-dependently increased CBF in WT mice, a response blocked by the TRPV1 antagonist SB366791. H2O2-induced vasodilation was significantly inhibited in db/db and V1KO mice. H2O2 caused robust
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s00395-016-0539-4" target="_blank" rel="noreferrer noopener">10.1007/s00395-016-0539-4</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).
*Coronary Circulation
*Microcirculation
2016
Animals
Basic research in cardiology
Bratz Ian N
Capsaicin
Chen Yeong-Renn
Connell Patrick J
Coronary blood flow
Damron Derek S
DelloStritto Daniel J
Department of Integrative Medical Sciences
Diabetic Angiopathies/*metabolism
Dick Gregory M
Fahmy Joseph N
Fancher Ibra S
HEK293 Cells
Humans
Hydrogen peroxide
Hydrogen Peroxide/*metabolism
Inbred C57BL
Kang Patrick T
Klarich Brittany
Knockout
Male
Mice
NEOMED College of Medicine
reactive oxygen species
Thodeti Charles K
TRPV Cation Channels/*metabolism
TRPV1
-
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.freeradbiomed.2016.09.021" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.freeradbiomed.2016.09.021</a>
Pages
10–19
Volume
101
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
4-Hydroxynonenal dependent alteration of TRPV1-mediated coronary microvascular signaling.
Publisher
An entity responsible for making the resource available
Free radical biology & medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-12
Subject
The topic of the resource
*4-Hydroxynonenal; *Coronary regulation; *Lipid peroxidation; *Post-translational modification; *Protein Processing; *Reactive oxygen species; *Signal Transduction; *TRPV1; Action Potentials/drug effects; Aldehydes/antagonists & inhibitors/metabolism/*pharmacology; Animal; Animals; Blood Flow Velocity; Calcium Signaling/drug effects; Capsaicin/*pharmacology; Cardiovascular Agents/*pharmacology; Coronary Circulation/drug effects; Coronary Vessels/metabolism/physiopathology; Cysteine/genetics/metabolism; Diabetes Mellitus/drug therapy/*metabolism/physiopathology; Disease Models; Femoral Artery/metabolism/physiopathology; HEK293 Cells; Humans; Inbred C57BL; Lipid Peroxidation; Male; Mice; Patch-Clamp Techniques; Post-Translational; TRPV Cation Channels/genetics/*metabolism; Vasodilation/drug effects
Creator
An entity primarily responsible for making the resource
DelloStritto Daniel J; Sinharoy Pritam; Connell Patrick J; Fahmy Joseph N; Cappelli Holly C; Thodeti Charles K; Geldenhuys Werner J; Damron Derek S; Bratz Ian N
Description
An account of the resource
We demonstrated previously that TRPV1-dependent regulation of coronary blood flow (CBF) is disrupted in diabetes. Further, we have shown that endothelial TRPV1 is differentially regulated, ultimately leading to the inactivation of TRPV1, when exposed to a prolonged pathophysiological oxidative environment. This environment has been shown to increase lipid peroxidation byproducts including
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.freeradbiomed.2016.09.021" target="_blank" rel="noreferrer noopener">10.1016/j.freeradbiomed.2016.09.021</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).
*4-Hydroxynonenal
*Coronary regulation
*Lipid peroxidation
*Post-translational modification
*Protein Processing
*Reactive oxygen species
*Signal Transduction
*TRPV1
2016
Action Potentials/drug effects
Aldehydes/antagonists & inhibitors/metabolism/*pharmacology
Animal
Animals
Blood Flow Velocity
Bratz Ian N
Calcium Signaling/drug effects
Cappelli Holly C
Capsaicin/*pharmacology
Cardiovascular Agents/*pharmacology
Connell Patrick J
Coronary Circulation/drug effects
Coronary Vessels/metabolism/physiopathology
Cysteine/genetics/metabolism
Damron Derek S
DelloStritto Daniel J
Department of Integrative Medical Sciences
Diabetes Mellitus/drug therapy/*metabolism/physiopathology
Disease Models
Fahmy Joseph N
Femoral Artery/metabolism/physiopathology
Free radical biology & medicine
Geldenhuys Werner J
HEK293 Cells
Humans
Inbred C57BL
Lipid Peroxidation
Male
Mice
NEOMED College of Medicine
Patch-Clamp Techniques
Post-Translational
Sinharoy Pritam
Thodeti Charles K
TRPV Cation Channels/genetics/*metabolism
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/10.1152/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
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).
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/10.1152/ajpheart.00082.2011" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00082.2011</a>
Pages
H1135–1142
Issue
3
Volume
301
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
Endothelin-mediated in vivo pressor responses following TRPV1 activation.
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
2011
2011-09
Subject
The topic of the resource
*Blood Pressure/drug effects; *Vasoconstriction/drug effects; Adrenergic alpha-Agonists/administration & dosage; Analysis of Variance; Animal; Animals; Azepines/administration & dosage; Biphenyl Compounds/administration & dosage; Capsaicin/administration & dosage; Cells; Cultured; Diabetes Mellitus; Diabetic Angiopathies/genetics/*metabolism/physiopathology; Dipeptides/administration & dosage; Disease Models; Dose-Response Relationship; Drug; Endothelial Cells/metabolism; Endothelin A Receptor Antagonists; Endothelin A/metabolism; Endothelin B Receptor Antagonists; Endothelin B/metabolism; Endothelin-1/*metabolism; Enzyme-Linked Immunosorbent Assay; Femoral Artery/drug effects/*metabolism/physiopathology; Inbred C57BL; Indoles/administration & dosage; Infusions; Intravenous; Knockout; Male; Mice; Phenylephrine/administration & dosage; Receptor; TRPV Cation Channels/agonists/deficiency/genetics/*metabolism; Type 2/genetics/*metabolism/physiopathology; Vasoconstrictor Agents/administration & dosage
Creator
An entity primarily responsible for making the resource
Ohanyan Vahagn A; Guarini Giacinta; Thodeti Charles K; Talasila Phani K; Raman Priya; Haney Rebecca M; Meszaros J Gary; Damron Derek S; Bratz Ian N
Description
An account of the resource
Transient receptor potential vanilliod 1 (TRPV1) channels have recently been postulated to play a role in the vascular complications/consequences associated with diabetes despite the fact that the mechanisms through which TRPV1 regulates vascular function are not fully known. Accordingly, our goal was to define the mechanisms by which TRPV1 channels modulate vascular function and contribute to vascular dysfunction in diabetes. We subjected mice lacking TRPV1 [TRPV1((-/-))], db/db, and control C57BLKS/J mice to in vivo infusion of the TRPV1 agonist capsaicin or the alpha-adrenergic agonist phenylephrine (PE) to examine the integrated circulatory actions of TRPV1. Capsaicin (1, 10, 20, and 100 mug/kg) dose dependently increased MAP in control mice (5.7 +/- 1.6, 11.7 +/- 2.1, 25.4 +/- 3.4, and 51.6 +/- 3.9%), which was attenuated in db/db mice (3.4 +/- 2.1, 3.9 +/- 2.1, 7.0 +/- 3.3, and 17.9 +/- 6.2%). TRPV1((-/-)) mice exhibited no changes in MAP in response to capsaicin, suggesting the actions of this agonist are specific to TRPV1 activation. Immunoblot analysis revealed decreased aortic TRPV1 protein expression in db/db compared with control mice. Capsaicin-induced responses were recorded following inhibition of endothelin A and B receptors (ET(A) /ET(B)). Inhibition of ET(A) receptors abolished the capsaicin-mediated increases in MAP. Combined antagonism of ET(A) and ET(B) receptors did not further inhibit the capsaicin response. Cultured endothelial cell exposure to capsaicin increased endothelin production as shown by an endothelin ELISA assay, which was attenuated by inhibition of TRPV1 or endothelin-converting enzyme. TRPV1 channels contribute to the regulation of vascular reactivity and MAP via production of endothelin and subsequent activation of vascular ET(A) receptors. Impairment of TRPV1 channel function may contribute to vascular dysfunction in diabetes.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00082.2011" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00082.2011</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).
*Blood Pressure/drug effects
*Vasoconstriction/drug effects
2011
Adrenergic alpha-Agonists/administration & dosage
American journal of physiology. Heart and circulatory physiology
Analysis of Variance
Animal
Animals
Azepines/administration & dosage
Biphenyl Compounds/administration & dosage
Bratz Ian N
Capsaicin/administration & dosage
Cells
Cultured
Damron Derek S
Department of Integrative Medical Sciences
Diabetes Mellitus
Diabetic Angiopathies/genetics/*metabolism/physiopathology
Dipeptides/administration & dosage
Disease Models
Dose-Response Relationship
Drug
Endothelial Cells/metabolism
Endothelin A Receptor Antagonists
Endothelin A/metabolism
Endothelin B Receptor Antagonists
Endothelin B/metabolism
Endothelin-1/*metabolism
Enzyme-Linked Immunosorbent Assay
Femoral Artery/drug effects/*metabolism/physiopathology
Guarini Giacinta
Haney Rebecca M
Inbred C57BL
Indoles/administration & dosage
Infusions
Intravenous
Knockout
Male
Meszaros J Gary
Mice
NEOMED College of Medicine
Ohanyan Vahagn A
Phenylephrine/administration & dosage
Raman Priya
Receptor
Talasila Phani K
Thodeti Charles K
TRPV Cation Channels/agonists/deficiency/genetics/*metabolism
Type 2/genetics/*metabolism/physiopathology
Vasoconstrictor Agents/administration & dosage
-
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/10.1371/journal.pone.0122189" target="_blank" rel="noreferrer noopener">http://doi.org/10.1371/journal.pone.0122189</a>
Pages
e0122189–e0122189
Issue
4
Volume
10
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
Propofol causes vasodilation in vivo via TRPA1 ion channels: role of nitric oxide and BKCa channels.
Publisher
An entity responsible for making the resource available
PloS one
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
1905-07
Subject
The topic of the resource
Female; Male; Animals; Mice; Signal Transduction; TRPA1 Cation Channel; Arterial Pressure/drug effects; Vasodilator Agents/*pharmacology; Propofol/*pharmacology; Transient Receptor Potential Channels/genetics/*metabolism; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits/*physiology; Nitric Oxide/*physiology; TRPV Cation Channels/genetics/metabolism; Inbred C57BL; Knockout; Drug Evaluation; Preclinical
Creator
An entity primarily responsible for making the resource
Sinha Sayantani; Sinharoy Pritam; Bratz Ian N; Damron Derek S
Description
An account of the resource
BACKGROUND: Transient receptor potential (TRP) ion channels of the A1 (TRPA1) and V1 (TRPV1) subtypes are key regulators of vasomotor tone. Propofol is an intravenous anesthetic known to cause vasorelaxation. Our objectives were to examine the extent to which TRPA1 and/or TRPV1 ion channels mediate propofol-induced depressor responses in vivo and to delineate the signaling pathway(s) involved. METHODS: Mice were subjected to surgery under 1.5-2.5% sevoflurane gas with supplemental oxygen. After a stable baseline in mean arterial pressure (MAP) was achieved propofol (2.5, 5.0, 10.0 mg/kg/min) was administered to assess the hemodynamic actions of the intravenous anesthetic. The effect of nitric oxide synthase (NOS) inhibition with L-NAME and/or calcium-gated K+ channel (BKCa) inhibition with Penetrim A (Pen A), alone and in combination, on propofol-induced decreases in mean arterial pressure were assessed in control C57Bl/6J, TRPA1-/-, TRPV1-/- and double-knockout mice (TRPAV-/-). RESULTS: Propofol decreased MAP in control mice and this effect was markedly attenuated in
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1371/journal.pone.0122189" target="_blank" rel="noreferrer noopener">10.1371/journal.pone.0122189</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
Animals
Arterial Pressure/drug effects
Bratz Ian N
Damron Derek S
Drug Evaluation
Female
Inbred C57BL
Knockout
Large-Conductance Calcium-Activated Potassium Channel alpha Subunits/*physiology
Male
Mice
Nitric Oxide/*physiology
PloS one
Preclinical
Propofol/*pharmacology
Signal Transduction
Sinha Sayantani
Sinharoy Pritam
Transient Receptor Potential Channels/genetics/*metabolism
TRPA1 Cation Channel
TRPV Cation Channels/genetics/metabolism
Vasodilator 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/10.1371/journal.pone.0180106" target="_blank" rel="noreferrer noopener">http://doi.org/10.1371/journal.pone.0180106</a>
Pages
e0180106–e0180106
Issue
6
Volume
12
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
TRPA1 and TRPV1 contribute to propofol-mediated antagonism of U46619-induced constriction in murine coronary arteries.
Publisher
An entity responsible for making the resource available
PloS one
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017
Subject
The topic of the resource
Male; Animals; Mice; TRPV Cation Channels/genetics/*metabolism; TRPA1 Cation Channel; Endothelial Cells/drug effects/metabolism; Nitric Oxide Synthase Type III/metabolism; Vasodilator Agents/*pharmacology; Coronary Vessels/*drug effects/metabolism; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits/metabolism; Microvessels/drug effects/metabolism; Propofol/*pharmacology; Transient Receptor Potential Channels/genetics/*metabolism; Vasoconstrictor Agents/antagonists & inhibitors/pharmacology; Vasodilation/drug effects/physiology; Cells; Cultured; Inbred C57BL; Knockout; 15-Hydroxy-11 alpha; 9 alpha-(epoxymethano)prosta-5; 13-dienoic Acid/*antagonists & inhibitors/pharmacology
Creator
An entity primarily responsible for making the resource
Sinharoy Pritam; Bratz Ian N; Sinha Sayantani; Showalter Loral E; Andrei Spencer R; Damron Derek S
Description
An account of the resource
BACKGROUND: Transient receptor potential (TRP) ion channels have emerged as key components contributing to vasoreactivity. Propofol, an anesthetic is associated with adverse side effects including hypotension and acute pain upon infusion. Our objective was to determine the extent to which TRPA1 and/or TRPV1 ion channels are involved in mediating propofol-induced vasorelaxation of mouse coronary arterioles in vitro and elucidate the potential cellular signal transduction pathway by which this occurs. METHODS: Hearts were excised from anesthetized mice and coronary arterioles were dissected from control C57Bl/6J, TRPA1-/-, TRPV1-/- and double-knockout mice (TRPAV-/-). Isolated microvessels were cannulated and secured in a temperature-controlled chamber and allowed to equilibrate for 1 hr. Vasoreactivity studies were performed in microvessels pre-constricted with U46619 to assess the dose-dependent relaxation effects of propofol on coronary microvascular tone. RESULTS: Propofol-induced relaxation was unaffected in vessels obtained from TRPV1-/- mice, markedly attenuated in pre-constricted vessels obtained from TRPA1-/- mice and abolished in vessels obtained from
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1371/journal.pone.0180106" target="_blank" rel="noreferrer noopener">10.1371/journal.pone.0180106</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).
13-dienoic Acid/*antagonists & inhibitors/pharmacology
15-Hydroxy-11 alpha
2017
9 alpha-(epoxymethano)prosta-5
Andrei Spencer R
Animals
Bratz Ian N
Cells
Coronary Vessels/*drug effects/metabolism
Cultured
Damron Derek S
Endothelial Cells/drug effects/metabolism
Inbred C57BL
Knockout
Large-Conductance Calcium-Activated Potassium Channel alpha Subunits/metabolism
Male
Mice
Microvessels/drug effects/metabolism
Nitric Oxide Synthase Type III/metabolism
PloS one
Propofol/*pharmacology
Showalter Loral E
Sinha Sayantani
Sinharoy Pritam
Transient Receptor Potential Channels/genetics/*metabolism
TRPA1 Cation Channel
TRPV Cation Channels/genetics/*metabolism
Vasoconstrictor Agents/antagonists & inhibitors/pharmacology
Vasodilation/drug effects/physiology
Vasodilator 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/10.1002/prp2.153" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/prp2.153</a>
Pages
e00153–e00153
Issue
4
Volume
3
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
Propofol restores TRPV1 sensitivity via a TRPA1-, nitric oxide synthase-dependent activation of PKCepsilon.
Publisher
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Pharmacology research & perspectives
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015-08
Subject
The topic of the resource
PKCepsilon and NOS; propofol; TRPA1; TRPV1
Creator
An entity primarily responsible for making the resource
Sinharoy Pritam; Zhang Hongyu; Sinha Sayantani; Prudner Bethany C; Bratz Ian N; Damron Derek S
Description
An account of the resource
We previously demonstrated that the intravenous anesthetic, propofol, restores the sensitivity of transient receptor potential vanilloid channel subtype-1 (TRPV1) receptors via a protein kinase C epsilon (PKCepsilon)-dependent and transient receptor potential ankyrin channel subtype-1 (TRPA1)-dependent pathway in sensory neurons. The extent to which the two pathways are directly linked or operating in parallel has not been determined. Using a molecular approach, our objectives of the current study were to confirm that TRPA1 activation directly results in PKCepsilon activation and to elucidate the cellular mechanism by which this occurs. F-11 cells were transfected with complimentary DNA (cDNA) for TRPV1 only or both TRPV1 and TRPA1. Intracellular Ca(2+) concentration was measured in individual cells via fluorescence microscopy. An immunoblot analysis of the total and phosphorylated forms of PKCepsilon, nitric oxide synthase (nNOS), and TRPV1 was also performed. In F-11 cells containing both channels, PKCepsilon inhibition prevented the propofol- and allyl isothiocyanate (AITC)-induced restoration of TRPV1 sensitivity to agonist stimulation as well as increased phosphorylation of PKCepsilon and TRPV1. In cells containing TRPV1 only, neither agonist induced PKCepsilon or TRPV1 phosphorylation. Moreover, NOS inhibition blocked propofol-and AITC-induced restoration of TRPV1 sensitivity and PKCepsilon phosphorylation, and PKCepsilon inhibition prevented the nitric oxide donor, SNAP, from restoring TRPV1 sensitivity. Also, propofol-and AITC-induced phosphorylation of nNOS and nitric oxide (NO) production were blocked with the
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/prp2.153" target="_blank" rel="noreferrer noopener">10.1002/prp2.153</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
Bratz Ian N
Damron Derek S
Pharmacology research & perspectives
PKCepsilon and NOS
propofol
Prudner Bethany C
Sinha Sayantani
Sinharoy Pritam
TRPA1
TRPV1
Zhang Hongyu
-
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/10.1097/ALN.0b013e31820dee67" target="_blank" rel="noreferrer noopener">http://doi.org/10.1097/ALN.0b013e31820dee67</a>
Pages
1169–1179
Issue
5
Volume
114
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
Propofol restores transient receptor potential vanilloid receptor subtype-1 sensitivity via activation of transient receptor potential ankyrin receptor subtype-1 in sensory neurons.
Publisher
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Anesthesiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2011
2011-05
Subject
The topic of the resource
Male; Mice; Capsaicin; Cells; Anesthetics; Animal Studies; Genes – Drug Effects; Carrier Proteins – Drug Effects; Carrier Proteins – Metabolism; Intravenous – Pharmacodynamics; Propofol – Pharmacodynamics; Sensory Receptor Cells – Drug Effects
Creator
An entity primarily responsible for making the resource
Zhang H; Wickley PJ; Sinha S; Bratz IN; Damron DS; Zhang Hongyu; Wickley Peter J; Sinha Sayantani; Bratz Ian N; Damron Derek S
Description
An account of the resource
Background: Cross talk between peripheral nociceptors belonging to the transient receptor potential vanilloid receptor subtype-1 (TRPV1) and ankyrin subtype-1 (TRPA1) family has been demonstrated recently. Moreover, the intravenous anesthetic propofol has directly activates TRPA1 receptors and indirectly restores sensitivity of TRPV1 receptors in dorsal root ganglion (DRG) sensory neurons. Our objective was to determine the extent to which TRPA1 activation is involved in mediating the propofol-induced restoration of TRPV1 sensitivity.Methods: Mouse DRG neurons were isolated by enzymatic dissociation and grown for 24 h. F-11 cells were transfected with complementary DNA for both TRPV1 and TRPA1 or TRPV1 only. The intracellular Ca concentration was measured in individual cells via fluorescence microscopy. After TRPV1 desensitization with capsaicin (100 nM), cells were treated with propofol (1, 5, and 10 μM) alone or with propofol in the presence of the TRPA1 antagonist, HC-030031 (0.5 μM), or the TRPA1 agonist, allyl isothiocyanate (AITC; 100 μM); capsaicin was then reapplied.Results: In DRG neurons that contain both TRPV1 and TRPA1, propofol and AITC restored TRPV1 sensitivity. However, in DRG neurons containing only TRPV1 receptors, exposure to propofol or AITC after desensitization did not restore capsaicin-induced TRPV1 sensitivity. Similarly, in F-11 cells transfected with both TRPV1 and TRPA1, propofol and AITC restored TRPV1 sensitivity. However, in F-11 cells transfected with TRPV1 only, neither propofol nor AITC was capable of restoring TRPV1 sensitivity.Conclusions: These data demonstrate that propofol restores TRPV1 sensitivity in primary DRG neurons and in cultured F-11 cells transfected with both the TRPV1 and TRPA1 receptors via a TRPA1-dependent process. Propofol's effects on sensory neurons may be clinically important and may contribute to peripheral sensitization to nociceptive stimuli in traumatized tissue.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1097/ALN.0b013e31820dee67" target="_blank" rel="noreferrer noopener">10.1097/ALN.0b013e31820dee67</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).
2011
Anesthesiology
Anesthetics
Animal Studies
Bratz Ian N
Bratz IN
Capsaicin
Carrier Proteins – Drug Effects
Carrier Proteins – Metabolism
Cells
Damron Derek S
Damron DS
Genes – Drug Effects
Intravenous – Pharmacodynamics
Male
Mice
Propofol – Pharmacodynamics
Sensory Receptor Cells – Drug Effects
Sinha S
Sinha Sayantani
Wickley Peter J
Wickley PJ
Zhang H
Zhang Hongyu