1
40
3
-
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.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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<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
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/10.2174/1381612811319130004" target="_blank" rel="noreferrer noopener">http://doi.org/10.2174/1381612811319130004</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
2366-2374
Issue
13
Volume
19
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
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
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Microvascular Function/dysfunction Downstream A Coronary Stenosis
Publisher
An entity responsible for making the resource available
Current Pharmaceutical Design
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013-04
Subject
The topic of the resource
artery disease; blood-flow; ca2+-activated k+ channels; Coronary microcirculation; coronary stenosis; endothelial dysfunction; flow-induced dilation; function; iib/iiia receptor blockade; left-ventricular wall; myocardial ischemia; myocardial-perfusion; nitric-oxide; Pharmacology & Pharmacy; resistive vessel; unstable angina
Creator
An entity primarily responsible for making the resource
Guarini G; Capozza P G; Huqi A; Morrone D; Chilian W M; Marzilli M
Description
An account of the resource
For decades coronary macrovascular atherosclerosis has been considered the principal manifestation of coronary heart disease, with most of our effort dedicated to identifying and removal of coronary stenosis. However, growing body of literature indicates that coronary microcirculation also contributes substantially to the pathophysiology of cardiovascular disease. An understanding of mechanisms regulating microvascular function is of critical importance in understanding its role in disease, especially because these regulatory mechanisms vary substantially across species, vascular bed and due to comorbidities. Indeed, the most obvious consequence of coronary stenosis is that it may limit blood supply to the dependent myocardium to the point of causing ischaemia during exercise or even at rest. However, this flow limiting effect is not only due to the passive hydraulic effect of a narrowed conduit, but also to active responses in the coronary microcirculation triggered by the presence of an epicardial stenosis. To understand this problem it is important to review the inter-related mechanisms that regulate flow to the left ventricular wall and modulate transmural distribution of flow. These regulatory mechanisms operate hierarchically and are heterogeneously distributed along the coronary vascular tree. It is also important to discuss the effect of myocardial performance in modulating both blood flow demands and coronary resistance. Some of the interactions between coronary stenosis and microcirculation are transient, like those documented in acute coronary syndromes or during percutaneous interventions. However, microcirculatory remodeling may be triggered by a chronic coronary stenosis, leading to a sustained impairment of blood supply even after successful removal of the epicardial stenosis. A deeper understanding of these phenomena may explain paradoxical findings in patients undergoing coronary revascularization, particularly when functional tests are used in their assessment. These aspects are discussed in detail in this review.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.2174/1381612811319130004" target="_blank" rel="noreferrer noopener">10.2174/1381612811319130004</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2013
artery disease
blood-flow
ca2+-activated k+ channels
Capozza P G
Chilian W M
Coronary microcirculation
coronary stenosis
Current Pharmaceutical Design
endothelial dysfunction
flow-induced dilation
Function
Guarini G
Huqi A
iib/iiia receptor blockade
Journal Article or Conference Abstract Publication
left-ventricular wall
Marzilli M
Morrone D
myocardial ischemia
myocardial-perfusion
nitric-oxide
Pharmacology & Pharmacy
resistive vessel
unstable angina