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.00731.2011" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00731.2011</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
H1410-H1422
Issue
7
Volume
302
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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
Biphasic Modulation Of The Mitochondrial Electron Transport Chain In Myocardial Ischemia And Reperfusion
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
2012-04
Subject
The topic of the resource
Cardiovascular System & Cardiology; cytochrome-c-oxidase; energy-metabolism; injury; nadh dehydrogenase; oxidative modification; oxygen-free-radicals; Physiology; postischemic myocardium; protein biosynthesis; rat-heart mitochondria; reactive oxygen species; transfer complex-i; translational control
Creator
An entity primarily responsible for making the resource
Lee H L; Chen C L; Yeh S T; Zweier J L; Chen Y R
Description
An account of the resource
Lee HL, Chen CL, Yeh ST, Zweier JL, Chen YR. Biphasic modulation of the mitochondrial electron transport chain in myocardial ischemia and reperfusion. Am J Physiol Heart Circ Physiol 302: H1410-H1422, 2012. First published January 20, 2012; doi: 10.1152/ajpheart.00731.2011.-Mitochondrial electron transport chain (ETC) is the major source of reactive oxygen species during myocardial ischemia-reperfusion (I/R) injury. Ischemic defect and reperfusion-induced injury to ETC are critical in the disease pathogenesis of postischemic heart. The properties of ETC were investigated in an isolated heart model of global I/R. Rat hearts were subjected to ischemia for 30 min followed by reperfusion for 1 h. Studies of mitochondrial function indicated a biphasic modulation of electron transfer activity (ETA) and ETC protein expression during I/R. Analysis of ETAs in the isolated mitochondria indicated that complexes I, II, III, and IV activities were diminished after 30 min of ischemia but increased upon restoration of flow. Immunoblotting analysis and ultrastructural analysis with transmission electron microscopy further revealed marked downregulation of ETC in the ischemic heart and then upregulation of ETC upon reperfusion. No significant difference in the mRNA expression level of ETC was detected between ischemic and postischemic hearts. However, reperfusion-induced ETC biosynthesis in myocardium can be inhibited by cycloheximide, indicating the involvement of translational control. Immunoblotting analysis of tissue homogenates revealed a similar profile in peroxisome proliferator-activated receptor-gamma coactivator-1 alpha expression, suggesting its essential role as an upstream regulator in controlling ETC biosynthesis during I/R. Significant impairment caused by ischemic and postischemic injury was observed in the complexes I-III. Analysis of NADH ferricyanide reductase activity indicated that injury of flavoprotein subcomplex accounts for 50% decline of intact complex I activity from ischemic heart. Taken together, our findings provide a new insight into the molecular mechanism of I/R-induced mitochondrial dysfunction.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00731.2011" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00731.2011</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2012
American Journal of Physiology-Heart and Circulatory Physiology
Cardiovascular System & Cardiology
Chen C L
Chen Y R
cytochrome-c-oxidase
energy-metabolism
Injury
Journal Article or Conference Abstract Publication
Lee H L
nadh dehydrogenase
oxidative modification
oxygen-free-radicals
Physiology
postischemic myocardium
Protein Biosynthesis
rat-heart mitochondria
reactive oxygen species
transfer complex-i
translational control
Yeh S T
Zweier J L
-
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.00282.2010" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00282.2010</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
H1938-H1949
Issue
5
Volume
300
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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
Angiotensin Type I Receptor Blockade In Conjunction With Enhanced Akt Activation Restores Coronary Collateral Growth In The Metabolic Syndrome
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
2011-05
Subject
The topic of the resource
Cardiovascular System & Cardiology; coronary artery occlusion; endothelial-cells; inhibition; ischemia-induced angiogenesis; kinase; mediated angiogenesis; nitric-oxide synthase; pathway; phosphorylation; Physiology; rat; smooth-muscle-cells; transient
Creator
An entity primarily responsible for making the resource
Jadhav R; Dodd T; Smith E; Bailey E; DeLucia A L; Russell J C; Madison R; Potter B; Walsh K; Jo H J; Rocic P
Description
An account of the resource
Jadhav R, Dodd T, Smith E, Bailey E, DeLucia AL, Russell JC, Madison R, Potter B, Walsh K, Jo H, Rocic P. Angiotensin type I receptor blockade in conjunction with enhanced Akt activation restores coronary collateral growth in the metabolic syndrome. Am J Physiol Heart Circ Physiol 300: H1938-H1949, 2011. First published February 18, 2011; doi:10.1152/ajpheart.00282.2010.-We have previously demonstrated that Akt was required for repetitive ischemia (RI)-induced coronary collateral growth (CCG) in healthy rats but was not activated by RI in the metabolic syndrome (JCR:LA-cp rats) where CCG was impaired. Here we hypothesized that failure of angiotensin type I receptor (AT(1)R) blockers to restore Akt activation is a key determinant of their inability to completely restore CCG in the metabolic syndrome. Therefore, we investigated whether adenovirus-mediated delivery of constitutively active Akt (MyrAkt-Adv.) in conjunction with AT(1)R blockade (candesartan) was able to restore RI-induced CCG in JCR:LA-cp rats. Successful myocardial MyrAkt-Adv delivery was confirmed by a >80% transduction efficiency and an approximately fourfold increase in Akt expression and activation. CCG was assessed by myocardial blood flow measurements in the normal and collateral-dependent zones. MyrAkt-Adv alone significantly increased RI-induced CCG in JCR:LA-cp rats (similar to 30%), but it completely restored CCG in conjunction with administration of candesartan. In contrast, dominant negative Akt (DN-Akt-Adv) reversed the beneficial effect of candesartan on CCG in JCR:LA-cp rats. We conclude that optimal restoration of coronary collateral growth in JCR:LA-cp rats requires a combination of AT(1)R blockade with constitutive Akt activation. These findings may carry implications for metabolic syndrome patients in need of coronary revascularization.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00282.2010" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00282.2010</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2011
American Journal of Physiology-Heart and Circulatory Physiology
Bailey E
Cardiovascular System & Cardiology
coronary artery occlusion
DeLucia A L
Dodd T
endothelial-cells
inhibition
ischemia-induced angiogenesis
Jadhav R
Jo H J
Journal Article or Conference Abstract Publication
Kinase
Madison R
mediated angiogenesis
nitric-oxide synthase
pathway
Phosphorylation
Physiology
Potter B
rat
Rocic P
Russell J C
Smith E
smooth-muscle-cells
transient
Walsh K
-
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
n/a
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
H1720-H1727
Issue
4
Volume
281
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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
Testosterone relaxes coronary arteries by opening the large-conductance, calcium-activated potassium channel
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
2001
2001-10
Subject
The topic of the resource
rat; vasodilation; ion channel; Physiology; Cardiovascular System & Cardiology; disease; smooth-muscle-cells; aorta; men; Vascular; hormones; androgen; steroid
Creator
An entity primarily responsible for making the resource
Deenadayalu V U P; White R E; Stallone J N; Gao X M; Garcia A J
Description
An account of the resource
Cardiovascular diseases are often considered to be a predominantly male health problem, and it has been suggested that testosterone exerts deleterious effects on cardiovascular function; however, few experimental studies support this suggestion. Moreover, the cellular and molecular mechanism(s) underlying vascular responses to testosterone is unknown. The present study has investigated the acute effects of testosterone on porcine coronary artery smooth muscle at the tissue and cellular levels. Contractile studies demonstrated that testosterone or dihydrotestosterone (a nonaromatizable metabolite) relaxed these arteries by an endothelium-independent mechanism involving potassium efflux. Direct evidence from patch-clamp studies confirmed that testosterone opened K+ channels in single coronary myocytes, and further analysis identified this protein as the large-conductance, calcium- and voltage-activated potassium (BKCa) channel. Moreover, inhibiting BKCa channel activity significantly attenuated testosterone-induced coronary relaxation. These findings indicate that testosterone relaxes porcine coronary arteries predominantly by opening BKCa channels in coronary myocytes, and this response may be associated with accumulation of cGMP. This novel mechanism may provide a better understanding of testosterone-induced vasorelaxation reported in recent experimental and early clinical studies.
Identifier
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n/a
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2001
American Journal of Physiology-Heart and Circulatory Physiology
androgen
Aorta
Cardiovascular System & Cardiology
Deenadayalu V U P
Disease
Gao X M
Garcia A J
Hormones
ion channel
Journal Article or Conference Abstract Publication
men
Physiology
rat
smooth-muscle-cells
Stallone J N
Steroid
Vascular
vasodilation
White R E
-
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.00019.2011" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00019.2011</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
H270-H277
Issue
1
Volume
302
Search for Full-text
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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
Optical mapping of cryoinjured rat myocardium grafted with mesenchymal stem 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
2012
2012-01
Subject
The topic of the resource
cardiomyocytes; Myocardial infarction; therapy; Physiology; Cardiovascular System & Cardiology; in-vitro; repair; Transplantation; phenotype; regeneration; infarction; heart; stem cell; action potential; pacemakers
Creator
An entity primarily responsible for making the resource
Costa A R; Panda N C; Yong S; Mayorga M E; Pawlowski G P; Fan K K; Penn M S; Laurita K R
Description
An account of the resource
Costa AR, Panda NC, Yong S, Mayorga ME, Pawlowski GP, Fan K, Penn MS, Laurita KR. Optical mapping of cryoinjured rat myocardium grafted with mesenchymal stem cells. Am J Physiol Heart Circ Physiol 302: H270-H277, 2012. First published October 28, 2011; doi: 10.1152/ajpheart.00019.2011.-Mesenchymal stem cells (MSCs) have been shown to improve cardiac electrophysiology when administered in the setting of acute myocardial infarction. However, the electrophysiological phenotype of MSCs in situ is not clear. We hypothesize that MSCs delivered intramyocardially to cryoinjured myocardium can engraft, but will not actively generate, action potentials. Cryoinjury-induced scar was created on the left ventricular epicardial surface of adult rat hearts. Within 30 min, hearts were injected with saline (sham, n = 11) or bone marrow-derived MSCs (2 x 10(6)) labeled with 1,1'-dioctadecyl-3,3,3,3'-tetramethyl-indocarbocyanine percholate (DiI; n = 16). At 3 wk, optical mapping and cell isolation were used to measure optical action potentials and calcium transients, respectively. Histological analysis confirmed subepicardial scar thickness and the presence of DiI-positive cells that express connexin-43. Optical action potential amplitude within the scar at MSC-positive sites (53.8 +/- 14.3%) was larger compared with sites devoid of MSCs (35.3 +/- 14.2%, P < 0.05) and sites within the scar of shams (33.5 +/- 6.9%, P < 0.05). Evidence of simultaneous action potential upstroke, the loss of action potential activity following ablation of adjacent viable myocardium, and no rapid calcium transient response in isolated DiI + cells suggest that the electrophysiological influence of engrafted MSCs is electrotonic. MSCs can engraft when directly injected into a cryoinjury and are associated with evidence of action potential activity. However, our results suggest that this activity is not due to generation of action potentials, but rather passive influence coupled from neighboring viable myocardium.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00019.2011" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00019.2011</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2012
action potential
American Journal of Physiology-Heart and Circulatory Physiology
cardiomyocytes
Cardiovascular System & Cardiology
Costa A R
Fan K K
heart
in-vitro
Infarction
Journal Article or Conference Abstract Publication
Laurita K R
Mayorga M E
myocardial infarction
pacemakers
Panda N C
Pawlowski G P
Penn M S
Phenotype
Physiology
Regeneration
repair
stem cell
therapy
Transplantation
Yong S
-
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.00694.2010" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00694.2010</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
H1069-H1077
Issue
3
Volume
300
Search for Full-text
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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
Endothelial NOS activity and myocardial oxygen metabolism define the salvageable ischemic time window for ischemic postconditioning
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
2011-03
Subject
The topic of the resource
cardioprotection; mice; inhibition; Physiology; Cardiovascular System & Cardiology; activation; dysfunction; reperfusion injury; tissue oxygenation; consumption; blood flow; electron paramagnetic resonance; infarct size; ischemia and reperfusion; mitochondrial enzyme activity; mitochondrial permeability transition; rabbit hearts; regional
Creator
An entity primarily responsible for making the resource
Cai M; Li Y J; Xu Y; Swartz H M; Chen C L; Chen Y R; He G L
Description
An account of the resource
Cai M, Li Y, Xu Y, Swartz HM, Chen C, Chen Y, He G. Endothelial NOS activity and myocardial oxygen metabolism define the salvageable ischemic time window for ischemic postconditioning. Am J Physiol Heart Circ Physiol 300: H1069-H1077, 2011. First published January 7, 2011; doi: 10.1152/ajpheart.00694.2010.-Ischemic postconditioning (IPOC) could be ineffective or even detrimental if the index ischemic duration is either too short or too long. The present study is to demonstrate that oxygen supply and metabolism defines a salvageable ischemic time window of IPOC in mice. C57BL/6 mice underwent coronary artery occlusion followed by reperfusion (I/R), with or without IPOC by three cycles of 10 s/10 s R/I. In vivo myocardial tissue oxygenation was monitored with electron paramagnetic resonance oximetry. Regional blood flow (RBF) was measured with a laser Doppler monitor. At the end of 60 min reperfusion, tissue from the risk area was collected, and mitochondrial enzyme activities were assayed. Tissue oximetry demonstrated that I/R induced a reperfusion hyperoxygenation state in the 30- and 45-min but not 15- and 60-min ischemia groups. IPOC attenuated the hyperoxygenation with 45 but not 30 min ischemia. RBF, eNOS phosphorylation, and mitochondrial enzyme activities were suppressed after I/R with different ischemic time, and IPOC afforded protection with 30 and 45 but not 60 min ischemia. Infarct size measurement indicated that IPOC reduced infarction with 30 and 45 min but not 60 min ischemia. Clearly, IPOC protected mouse heart with a defined ischemic time window between 30 and 45 min. This salvageable time window was accompanied by the improvement of RBF due to increased phosphorylated eNOS and the preservation of mitochondrial oxygen consumption due to conserved mitochondrial enzyme activities. Interestingly, this salvageable ischemic time window was mirrored by tissue hyperoxygenation status in the postischemic heart.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00694.2010" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00694.2010</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2011
activation
American Journal of Physiology-Heart and Circulatory Physiology
blood flow
Cai M
cardioprotection
Cardiovascular System & Cardiology
Chen C L
Chen Y R
consumption
dysfunction
electron paramagnetic resonance
He G L
infarct size
inhibition
ischemia and reperfusion
Journal Article or Conference Abstract Publication
Li Y J
Mice
mitochondrial enzyme activity
mitochondrial permeability transition
Physiology
rabbit hearts
regional
Reperfusion Injury
Swartz H M
tissue oxygenation
Xu Y
-
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.00876.2009" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00876.2009</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
H966-H973
Issue
3
Volume
298
Search for Full-text
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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
Contribution of BKCa channels to local metabolic coronary vasodilation: effects of metabolic syndrome
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
2010
2010-03
Subject
The topic of the resource
exercise; Physiology; Cardiovascular System & Cardiology; nitric-oxide; blood flow; coronary blood flow; smooth-muscle-cells; insulin-resistance; cardiovascular-disease; pigs; ca2+-activated k+ channels; induced relaxation; Ossabaw miniature swine; A; diabetic dyslipidemic; exercising dogs; myocardial oxygen consumption; myocardial-metabolism; penitrem
Creator
An entity primarily responsible for making the resource
Borbouse L; Dick G M; Payne G A; Payne B D; Svendsen M C; Neeb Z P; Alloosh M; Bratz I N; Sturek M; Tune J D
Description
An account of the resource
Borbouse L, Dick GM, Payne GA, Payne BD, Svendsen MC, Neeb ZP, Alloosh M, Bratz IN, Sturek M, Tune JD. Contribution of BKCa channels to local metabolic coronary vasodilation: effects of metabolic syndrome. Am J Physiol Heart Circ Physiol 298: H966-H973, 2010. First published December 31, 2009; doi:10.1152/ajpheart.00876.2009.-This investigation was designed to examine the hypothesis that impaired function of coronary microvascular large-conductance Ca2+-activated K+ (BKCa) channels in metabolic syndrome (MetS) significantly attenuates the balance between myocardial oxygen delivery and metabolism at rest and during exercise-induced increases in myocardial oxygen consumption (M(V) over dotO(2)). Studies were conducted in conscious, chronically instrumented Ossabaw swine fed a normal maintenance diet (11% kcal from fat) or an excess calorie atherogenic diet (43% kcal from fat, 2% cholesterol, 20% kcal from fructose) that induces many common features of MetS. Data were collected under baseline/resting conditions and during graded treadmill exercise before and after selective blockade of BKCa channels with penitrem A (10 mu g/kg iv). We found that the exercise-induced increases in blood pressure were significantly elevated in MetS swine. No differences in baseline cardiac function or heart rate were noted. Induction of MetS produced a parallel downward shift in the relationship between coronary venous PO2 and M(V) over dotO(2) (P < 0.001) that was accompanied by a marked release of lactate (negative lactate uptake) as M(V) over dotO(2) was increased with exercise (P < 0.005). Inhibition of BKCa channels with penitrem A did not significantly affect blood pressure, heart rate, or the relationship between coronary venous PO2 and M(V) over dotO(2) in lean or MetS swine. These data indicate that BKCa channels are not required for local metabolic control of coronary blood flow under physiological (lean) or pathophysiological (MetS) conditions. Therefore, diminished function of BKCa channels does not contribute to the impairment of myocardial oxygen-supply demand balance in MetS.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00876.2009" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00876.2009</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2010
A
Alloosh M
American Journal of Physiology-Heart and Circulatory Physiology
blood flow
Borbouse L
Bratz I N
ca2+-activated k+ channels
Cardiovascular System & Cardiology
cardiovascular-disease
Coronary blood flow
diabetic dyslipidemic
Dick G M
Exercise
exercising dogs
induced relaxation
insulin-resistance
Journal Article or Conference Abstract Publication
myocardial oxygen consumption
myocardial-metabolism
Neeb Z P
nitric-oxide
Ossabaw miniature swine
Payne B D
Payne G A
penitrem
Physiology
pigs
smooth-muscle-cells
Sturek M
Svendsen M C
Tune J D
-
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.00888.2009" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00888.2009</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
H1182-H1189
Issue
4
Volume
298
Search for Full-text
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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
Metabolic syndrome reduces the contribution of K+ channels to ischemic coronary vasodilation
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
2010
2010-04
Subject
The topic of the resource
potassium channels; exercise; Physiology; Cardiovascular System & Cardiology; blood flow; activation; smooth-muscle-cells; heart; adenosine; adenosine triphosphate-dependent; arterioles; calcium-activated potassium channels; cardiovascular-disease mortality; coronary reactive hyperemia; myocardial reactive hyperemia; Ossabaw miniature swine; sensitive potassium channels; type 2 diabetes; voltage-activated potassium channels
Creator
An entity primarily responsible for making the resource
Borbouse L; Dick G M; Payne G A; Berwick Z C; Neeb Z P; Alloosh M; Bratz I N; Sturek M; Tune J D
Description
An account of the resource
Borbouse L, Dick GM, Payne GA, Berwick ZC, Neeb ZP, Alloosh M, Bratz IN, Sturek M, Tune JD. Metabolic syndrome reduces the contribution of K+ channels to ischemic coronary vasodilation. Am J Physiol Heart Circ Physiol 298: H1182-H1189, 2010. First published January 29, 2010; doi: 10.1152/ajpheart.00888.2009.-This investigation tested the hypothesis that metabolic syndrome decreases the relative contribution of specific K+ channels to coronary reactive hyperemia. Ca2+-activated (BKCa), voltage-activated (K-V), and ATP-dependent (K-ATP) K+ channels were investigated. Studies were conducted in anesthetized miniature Ossabaw swine fed a normal maintenance diet (11% kcal from fat) or an excess calorie atherogenic diet (43% kcal from fat, 2% cholesterol, 20% kcal from fructose) for 20 wk. The latter diet induces metabolic syndrome, increasing body weight, fasting glucose, total cholesterol, and triglyceride levels. Ischemic vasodilation was determined by the coronary flow response to a 15-s occlusion before and after cumulative administration of antagonists for BKCa (penitrem A; 10 mu g/kg iv), K-V (4-aminopyridine; 0.3 mg/kg iv) and K-ATP (glibenclamide; 1 mg/kg iv) channels. Coronary reactive hyperemia was diminished by metabolic syndrome as the repayment of flow debt was reduced similar to 30% compared with lean swine. Inhibition of BKCa channels had no effect on reactive hyperemia in either lean or metabolic syndrome swine. Subsequent inhibition of KV channels significantly reduced the repayment of flow debt (similar to 25%) in both lean and metabolic syndrome swine. Additional blockade of K-ATP channels further diminished (similar to 45%) the repayment of flow debt in lean but not metabolic syndrome swine. These data indicate that the metabolic syndrome impairs coronary vasodilation in response to cardiac ischemia via reductions in the contribution of K+ channels to reactive hyperemia.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00888.2009" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00888.2009</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2010
activation
adenosine
adenosine triphosphate-dependent
Alloosh M
American Journal of Physiology-Heart and Circulatory Physiology
Arterioles
Berwick Z C
blood flow
Borbouse L
Bratz I N
calcium-activated potassium channels
Cardiovascular System & Cardiology
cardiovascular-disease mortality
coronary reactive hyperemia
Dick G M
Exercise
heart
Journal Article or Conference Abstract Publication
myocardial reactive hyperemia
Neeb Z P
Ossabaw miniature swine
Payne G A
Physiology
Potassium Channels
sensitive potassium channels
smooth-muscle-cells
Sturek M
Tune J D
Type 2 diabetes
voltage-activated potassium channels
-
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.00466.2009" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00466.2009</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
H1629-H1637
Issue
5
Volume
297
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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
Impaired function of coronary BKCa channels in metabolic syndrome
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
2009
2009-11
Subject
The topic of the resource
obesity; Physiology; Cardiovascular System & Cardiology; channels; smooth-muscle-cells; circulation; cardiovascular-disease; Ion channels; beta-1 subunit; activated potassium; arteriolar dilation; blood flow; ca2+-activated k+ channels; currents; diabetic fatty rats; induced relaxation; large-conductance; outward
Creator
An entity primarily responsible for making the resource
Borbouse L; Dick G M; Asano S; Bender S B; Dincer U D; Payne G A; Neeb Z P; Bratz I N; Sturek M; Tune J D
Description
An account of the resource
Borbouse L, Dick GM, Asano S, Bender SB, Dincer UD, Payne GA, Neeb ZP, Bratz IN, Sturek M, Tune JD. Impaired function of coronary BKCa channels in metabolic syndrome. Am J Physiol Heart Circ Physiol 297: H1629-H1637, 2009. First published September 11, 2009; doi:10.1152/ajpheart.00466.2009.-The role of large-conductance Ca2+-activated K+ (BKCa) channels in regulation of coronary microvascular function is widely appreciated, but molecular and functional changes underlying the deleterious influence of metabolic syndrome (MetS) have not been determined. Male Ossabaw miniature swine consumed for 3-6 mo a normal diet (11% kcal from fat) or an excess-calorie atherogenic diet that induces MetS (45% kcal from fat, 2% cholesterol, 20% kcal from fructose). MetS significantly impaired coronary vasodilation to the BKCa opener NS-1619 in vivo (30-100 mu g) and reduced the contribution of these channels to adenosine-induced microvascular vasodilation in vitro (1-100 mu M). MetS reduced whole cell penitrem A (1 mu M)-sensitive K+ current and NS-1619-activated (10 mu M) current in isolated coronary vascular smooth muscle cells. MetS increased the concentration of free intracellular Ca2+ and augmented coronary vasoconstriction to the L-type Ca2+ channel agonist BAY K 8644 (10 pM-10 nM). BKCa channel alpha and beta(1) protein expression was increased in coronary arteries from MetS swine. Coronary vascular dysfunction in MetS is related to impaired BKCa channel function and is accompanied by significant increases in L-type Ca2+ channel-mediated coronary vasoconstriction.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00466.2009" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00466.2009</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2009
activated potassium
American Journal of Physiology-Heart and Circulatory Physiology
arteriolar dilation
Asano S
Bender S B
beta-1 subunit
blood flow
Borbouse L
Bratz I N
ca2+-activated k+ channels
Cardiovascular System & Cardiology
cardiovascular-disease
channels
Circulation
currents
diabetic fatty rats
Dick G M
Dincer U D
induced relaxation
Ion Channels
Journal Article or Conference Abstract Publication
large-conductance
Neeb Z P
Obesity
outward
Payne G A
Physiology
smooth-muscle-cells
Sturek M
Tune J D
-
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.00911.2013" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00911.2013</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
H1032-H1040
Issue
7
Volume
306
Search for Full-text
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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
Novel role of aminopeptidase-A in angiotensin-(1-7) metabolism post myocardial infarction
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
2014
2014-04
Subject
The topic of the resource
ace2; Aminopeptidase A; angiotensin peptides; antihypertensive agents; carboxypeptidase; Cardiovascular System & Cardiology; enzyme; inhibitors; kidney; MALDI-imaging; mass-spectrometry; Myocardial infarction; Physiology; renal damage; renin-angiotensin system; spontaneously hypertensive-rats; system
Creator
An entity primarily responsible for making the resource
Alghamri M S; Morris M; Meszaros J G; Elased K M; Grobe N
Description
An account of the resource
Aminopeptidase-A (APA) is a less well-studied enzyme of the renin-angiotensin system. We propose that it is involved in cardiac angiotensin (ANG) metabolism and its pathologies. ANG-(1-7) can ameliorate remodeling after myocardial injury. The aims of this study are to 1) develop mass spectrometric (MS) approaches for the assessment of ANG processing by APA within the myocardium; and 2) investigate the role of APA in cardiac ANG-(1-7) metabolism after myocardial infarction (MI) using sensitive MS techniques. MI was induced in C57Bl/6 male mice by ligating the left anterior descending (LAD) artery. Frozen mouse heart sections (in situ assay) or myocardial homogenates (in vitro assay) were incubated with the endogenous APA substrate, ANG II. Results showed concentration-and time-dependent cardiac formation of ANG III from ANG II, which was inhibited by the specific APA inhibitor, 4-amino-4-phosphonobutyric acid. Myocardial APA activity was significantly increased 24 h after LAD ligation (0.82 +/- 0.02 vs. 0.32 +/- 0.02 rho mol.min(-1).mu g(-1), MI vs. sham, P < 0.01). Both MS enzyme assays identified the presence of a new peptide, ANG-(2-7), m/z 784, which accumulated in the MI (146.45 +/- 6.4 vs. 72.96 +/- 7.0%, MI vs. sham, P < 0.05). Use of recombinant APA enzyme revealed that APA is responsible for ANG-(2-7) formation from ANG-(1-7). APA exhibited similar substrate affinity for ANG-(1-7) compared with ANG II {K-m (ANG II) = 14.67 +/- 1.6 vs. K-m [ANG-(1-7)] = 6.07 +/- 1.12 mu mol/l, P < 0.05}. Results demonstrate a novel role of APA in ANG-(1-7) metabolism and suggest that the upregulation of APA, which occurs after MI, may deprive the heart of cardioprotective ANG-(1-7). Thus APA may serve as a potentially novel therapeutic target for management of tissue remodeling after MI.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00911.2013" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00911.2013</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2014
ace2
Alghamri M S
American Journal of Physiology-Heart and Circulatory Physiology
Aminopeptidase A
angiotensin peptides
antihypertensive agents
carboxypeptidase
Cardiovascular System & Cardiology
Elased K M
enzyme
Grobe N
inhibitors
Journal Article or Conference Abstract Publication
Kidney
MALDI-imaging
Mass-spectrometry
Meszaros J G
Morris M
myocardial infarction
Physiology
renal damage
renin-angiotensin system
spontaneously hypertensive-rats
system
-
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.1997.273.5.h2155" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.1997.273.5.h2155</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
H2155-H2160
Issue
5
Volume
273
Search for Full-text
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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
Effects of ionic channel antagonists barium, cesium, and UL-FS-49 on vagal slowing of atrial rate in dogs
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
1997
1997-11
Subject
The topic of the resource
acetylcholine; atrioventricular nodes; autonomic nervous system; block; cardiac pacemaker; Cardiovascular System & Cardiology; cat; current if; heart rate; ionic currents; pacemaker activity; parasympathetic; Physiology; purkinje-fibers; sinoatrial node cells; sinus node; stimulation; vagus nerves
Creator
An entity primarily responsible for making the resource
Wallick D W; Kuguoglu A; Yang T N; Stuesse S L; Levy M N
Description
An account of the resource
In response to a brief vagal stimulus, the atrial rate initially slows, then transiently accelerates, and slows a second time. We determined the effects of three antagonists to two ionic channels on this characteristic triphasic pacemaker response. Brief bursts of vagal stimulation were delivered to anesthetized dogs, and atrial cycle lengths were recorded. Either barium, cesium, or UL-FS-49 was administered. Barium, which primarily blocks the acetylcholine-sensitive potassium current (I-K,I-ACh), attenuated the initial vagally induced bradycardia by >50% without affecting the subsequent acceleration or the secondary slowing. Cesium and UL-FS-49 [both of which primarily block the pacemaker current (I-f)] did not affect the initial vagal slowing of atrial rate but abolished the acceleratory portion of the response. The secondary slowing was abolished by cesium but not by UL-FS-49. We conclude that the initial rapid atrial response to acetylcholine is mediated mainly by the I-K,I-ACh, with little contribution from the I-f. The subsequent acceleration is mediated by activation of the I-f.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.1997.273.5.h2155" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.1997.273.5.h2155</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
1997
Acetylcholine
American Journal of Physiology-Heart and Circulatory Physiology
atrioventricular nodes
autonomic nervous system
block
cardiac pacemaker
Cardiovascular System & Cardiology
cat
current if
Heart Rate
ionic currents
Journal Article
Kuguoglu A
Levy M N
pacemaker activity
parasympathetic
Physiology
purkinje-fibers
sinoatrial node cells
sinus node
Stimulation
Stuesse S L
vagus nerves
Wallick D W
Yang T N
-
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.00421.2002" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00421.2002</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
H176-H184
Issue
1
Volume
284
Search for Full-text
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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
Aldosterone stimulates proliferation of cardiac fibroblasts by activating Ki-RasA and MAPK1/2 signaling
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
2003
2003-01
Subject
The topic of the resource
angiotensin-ii; Cardiovascular System & Cardiology; differentiation; fibrosis; gene-expression; Heart failure; identification; induction; Kirsten Ras; mineralocorticoid; mitogen-activated protein kinase; myofibroblast; na+ reabsorption; Physiology; receptor; spironolactone; transcription
Creator
An entity primarily responsible for making the resource
Stockand J D; Meszaros J G
Description
An account of the resource
Aldosterone plays a pathological role in cardiac fibrosis by directly affecting cardiac fibroblasts. Understanding of the cellular mechanisms of aldosterone action in cardiac fibroblasts, however, is rudimentary. One possibility is that aldosterone promotes proliferation of cardiac fibroblasts by activating specific cellular signaling cascades. The current study tests whether aldosterone stimulates proliferation of isolated adult rat cardiac myofibroblasts (RCF) by activating Kirsten Ras (Ki-RasA) and its effector, the MAPK1/2 cascade. Aldosterone (10 nM) significantly increased RCF proliferation. This action was sensitive to the mineralocorticoid receptor (MR) antagonist spironolactone. Expression of MR in RCF and the whole rat heart was confirmed by immunoblotting. Aldosterone significantly increased absolute and active (GTP bound) Ki-RasA levels in RCF. Aldosterone, in addition, significantly increased phospho-c-Raf and phospho-MAPK1/2. The effects of aldosterone on Ki-RasA and phospho-c-Raf proteins were inhibited by spironolactone but not RU-486, suggesting that aldosterone acts via MR. Inhibitors of MEK1/2 and c-Raf prevented aldosterone-induced activation of MAPK1/2 and proliferation. These results show that aldosterone directly increases RCF proliferation through MR-dependent activation of Ki-RasA and its effector, the MAPK1/2 cascade. Activation of cardiac fibroblasts through such a cascade may play a role in the pathological actions exerted by aldosterone on the heart.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00421.2002" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00421.2002</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2003
American Journal of Physiology-Heart and Circulatory Physiology
angiotensin-ii
Cardiovascular System & Cardiology
differentiation
Fibrosis
gene-expression
Heart failure
identification
induction
Journal Article
Kirsten Ras
Meszaros J G
mineralocorticoid
mitogen-activated protein kinase
myofibroblast
na+ reabsorption
Physiology
Receptor
spironolactone
Stockand J D
Transcription